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Muscular System
Chapter 10 p.274
Introduction
The bones provide the levers and structure of the skeleton but it is
the muscles that cause the movement.
Motion results from the contraction and relaxation of muscles.
The muscles change chemical energy (ATP) into mechanical
energy to generate force, perform work and produce movement.
• Muscles account for 40-50% of total body weight.
• The scientific study of muscles is known as myology.
Functions of Muscle Tissue
Muscle tissues have a specialized property- contractility, the
capability of shortening.
Through the contraction and relaxation of muscles, 4 functions
can be described:
Fig. 10.1 p276, p 274
1. Motion such as walking, running, grasping.
These movements rely on the integrated function of bones,
joints, and skeletal muscles (as well as the nervous system).
The muscles are connected to the skeleton and pull to cause
movement.
Mostly voluntary.
2. Propulsion of materials through the body (blood, ingested
food, sperm, ova, urine).
Examples: Cardiac muscle contracts to pump blood to
all body tissues.
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Smooth muscle contractions aid in the movement of
food through the GI tract, urine through urinary system.
Skeletal muscle (squeezing upon contraction) helps
return venous blood and lymph to the heart.
3. Maintain body posture and sphincter control.
Examples: Skeletal muscle (antagonistic) contractions maintain
the body in stable positions as a when standing, an example of
muscle tension without movement.
Sustained contraction of smooth muscles (sphincters) prevent
outflow of contents of a hollow organ, as in the urinary bladder,
colon, or stomach.
4. Thermogenesis (generating heat).
Heat is a byproduct of muscle contraction. Muscle generates
about 85% of body heat.
Fig 10.11 p 251
When more heat is needed to maintain body temperature,
involuntary muscle contraction (shivering), can increase
thermogenesis by several 100%.
Smooth muscle in arteriole wall will contract to conserve heat
and relax to increase blood flow to the skin and remove heat
from the body.
Contractile Proteins
Movement in living cells involves special protein molecules,
contractile proteins.
Contractile proteins can convert chemical energy in ATP, into the
mechanical energy of motion.
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Surprisingly, contractile proteins have been found in many types
of cells other than muscle cells. They account for things like:
1. Movement of chromosomes in cell division.
2. Movement of WBCs (and mitochondria).
3. Movement of cilia and flagella (as in sperm).
Therefore, muscle tissue is not unique in its possession of
contractile proteins but muscle tissue is distinguished by its high
concentration of contractile proteins.
Types of Muscle Tissue
p 274
There are 3 types of muscle tissue:
1. Skeletal muscle.
2. Smooth (visceral) muscle.
3. Cardiac muscle.
Let's look at the 3 types of muscle tissue more closely.
1. Skeletal Muscle
Is the muscle that is typically attached to the skeleton and is
responsible for movement:
a. of the skeleton.
b. of the diaphragm in breathing.
c. Sphincters
Circles of skeletal muscle important in voluntary release
of urine and feces.
• Contraction of skeletal muscle occurs by way of nerve
impulses. (somatic motor neurons).
• You have voluntary control of the contraction of skeletal
muscle. Therefore sometimes called, voluntary muscle.
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• Skeletal muscle is the largest tissue of the body, approximately
40% of body weight.
2. Smooth (visceral) muscle
• Visceral refers to internal organs of chest and abdomen.
• Smooth muscle surrounds the hollow tubes and chambers of
the body.
• Found in organs of digestive system, reproductive, urinary, and
blood vessels.
• Also found in skin attached to hair follicles.
• Smooth muscle functions to propel things through tubes
(peristalsis = wave like contractions).
• May change size (diameter) of an organ, important in
maintaining proper blood flow and pressure.
Do you have voluntary control over contraction of smooth muscle?
No. Involuntary muscle.
Contraction of smooth muscle is inherent (automatic or involuntary).
There are several types of control vs. skeletal muscle.
Contraction of smooth muscle may be altered by:
p298-9
a. Physical stimulus:
• Stretching initially causes contraction followed by
relaxation with continued tension on contents of tubing, so
pressure remains constant. Allows tubing to lengthen
while maintaining pressure. Called stress-relaxation
response.
b. Chemicals
c. Nerves (via neurotransmitters) creating action potentials
mainly from the Autonomic Nervous System (ANS).
• Visceral muscle action potentials are spread to
neighboring muscle fibers thru gap junctions.
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• In multiunit muscle tissue, only the muscle fibers touched
by a nerve contract. Example: walls of larger arteries,
airways, arrector pilli
d. Hormones
• Examples: e.g. epinephrine from adrenal medulla relaxes
airways).
e. Local changes (temperature, pH, O2, CO2).
3. Cardiac muscle
• Cardiac muscle is the muscle of the heart.
• It serves to pump (propel) the blood.
• Cardiac muscle contractions are inherent (originate in the
heart not nervous system) and includes a pacemaker that
causes the heart to beat. Autorhythmic.
• The heart rate may be modulated by ANS nerves
(neurotransmitters) and other chemicals (hormones:
epinephrine and norepinephrine speed up, Ca++
strengthens contraction).
• Cardiac and smooth muscle together makeup about 10%
of body weight.
Note:
In this section we primarily will discuss skeletal muscle and to a lessor
extent smooth muscle.
We will discuss heart muscle further when we get to the cardiovascular
system.
Microscopic Functional (Physiologic) Anatomy of Skeletal
Muscle
fig. 10.1, p. 276.
Introduction
• There are 600 skeletal muscles that have been identified on
the human body.
• They are attached to bone by bundles of C.T. called
tendons. These allow the muscles to pull bones closer
together.
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• If we examine a skeletal muscle we see that it is composed
of bundles of elongated cells or fibers.
o Terminology: A Muscles cell = muscle fiber.
Muscle
Let's examine the structural organization of a skeletal muscle:
Use figure 10.1 p 276
Muscle
• A skeletal muscle is surrounded by dense, irregular C.T.
called deep fascia that strengthens and protects the muscle.
• The C.T. enclosure allows for free movement of muscle.
• Between muscle fibers are collagen, elastic fibers, nerves,
and blood vessels.
• The dense C.T. extends beyond the muscle at each end to
form a tendon that attaches to periosteum of a bone.
o Example: calcaneal (Achilles) tendon of gastrocnemius/soleus
muscles in the calf attaches to the calcaneus bone of the foot.
Muscle Fiber = Muscle Cell = Myofiber
Use figure 10.1
Individual muscle fibers run longitudinally (parallel to each other)
through the muscle. They number from 100s to 1000s in a
muscle.
Muscle fiber longitudinal section notes
Fig 10.3 p 278
Note the longitudinal muscle fiber (muscle cell or myofiber)
showing cross striations, nucleus, and myofibrils.
• A longitudinal muscle fiber (myofiber) is very long.
o Typically 100 um (but up to 30 cm) in length, cylindrical cells,
diameter 10-100 um.
• It is one of largest cells in the body.
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o It is formed from many myoblasts during development,
so really started out as many cells. Each cell has
numerous nuclei located in the periphery, out of the way of
contraction apparatus.
• Mitochondria lie in rows along the muscle contractile proteins
that need ATP to drive contraction events.
Muscle cell (fiber) x-section
Use figure 10.3 p278
Note the cross section of muscle fiber showing nuclei at cell
periphery, sarcoplasm (muscle cell cytoplasm), myofibrils,
sarcolemma (muscle cell membrane).
• Notice the nuclei are at the periphery out of the way of the
contractile elements.
• Does the nucleus have a difficult time controlling such a
large cell?
o No, they are multinucleate!
• The plasma membrane is called the sarcolemma. Sarkos =
flesh, lemma = sheath
• The cytoplasm is called sarcoplasm.
• The muscle fiber (cell) is stuffed with tiny threads called
myofibrils that contain the contractile proteins.
o They extend lengthwise within the muscle fiber.
o They stain with alternating light and dark bands giving a striated
appearance.
o These bands are called cross-striations, which give rise the
reference to striated muscle.
• Myofibril = contractile elements of skeletal muscle
o They shorten to cause movement when stimulated by a neuron.
o 1-2 um in diameter consisting of 3 filament types. These will be
discussed soon.
Myofibril Showing Sarcomere
Use figure 10.4, 10.5 p. 280.
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Note the longitudinal section of a myofibril showing striations
containing A band (dark), I band (light), sarcomere.
• When a myofibril is stained, you can see alternating light and
dark bands which appear as striations.
o Light = I band (isotropic = scatters light evenly under
microscope).
o Dark band = A band (anisotropic = scatters light unevenly under
microscope).
• Each myofibril is made up of a longitudinal series of
repeated units called sarcomeres.
• We will soon see these are the basic functional unit for
contraction in striated muscle.
Higher magnification of a myofibril showing 2 sarcomeres
Use fig. 10.4 and 10.5. p 280
Note the appearance of 1 or 2 sarcomeres showing the
sarcomere, Z disc (line), H zone (band), I band, and A band.
This diagram shows the relaxed, uncontracted state of the
sarcomere.
• A myofibril at the molecular level is made up of
myofilaments = contractile proteins.
See Fig. 10.6 p281 also
• There are 2 major contractile proteins:
o 1. Myosin- thick filaments
16 nm diameter. MW = 500,000. 200 molecules/ thick
filament.
They are shaped similar to a golf club with a long tail with
a club like head.
The tails point toward the center of the sarcomere (M
line).
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o 2. Actin- thin filaments Globular protein polymerized to
form ling filaments. Two of these intertwine to form the
thin filament.
8 nm diameter. MW = 60,000.
Anchored at the Z discs at each end of sarcomere.
2 other proteins are associated with the thin filament:
• Tropomyosin
• Troponin.
• They perform a regulatory role in contraction and
will be will be discussed later.
• A band (dark band in middle of sarcomere)
o It is located centrally within a sarcomere.
o Consists mostly of thick filaments (myosin) and portions of thin
filaments (actin) that overlap thick filaments. See the ‘zone of
overlap’ fig 10.4.
o This creates a dark, dense appearance.
• I band (light bands at each end of sarcomere)
o Straddles the Z disc at the end of each sarcomere, so it
overlaps with the adjacent sarcomere.
o Consists of the rest of the thin filaments (actin) only. No thick
filaments.
• Z disc (lines) (narrow, plate shaped region)
o The Z disc passes through the center of each I band (light),
anchors the thin filaments.
o It separates one sarcomere from another.
• H zone H= helles, German for clear
o The narrow H zone in the center of each A band (dark) contains
thick but not thin filaments.
• M line M= middle
o The M line runs through the H zone and is the attachment point
of adjacent thick filaments.
Elastic filaments
See figure 10.4 to demonstrate the elastic filament.
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• The 3rd most common muscle protein is a non contractile
filament, the elastic filament.
• It is composed of the stretchy protein called titan (connectin)
(huge MW of 3 million Daltons, largest protein with > 25k
amino acids).
• It anchors the thick filament to the Z disc and then invades
the M line to stabilize its structure.
• The portion that extends through and is exposed in the I
band is highly elastic. It can stretch up to 4x and return to
resting length without harm.
• They are relaxed in the resting sarcomere.
• It is responsible for the muscle’s ability to spring back into
shape after being stretched by an external force.
• Plays a major role in the precise organization of the A band.
• Or in other words, maintains the normal alignment of the
thick and thin filaments.
Other proteins
• Myomesin forms the M line that binds thick to titan
• Dystrophin is a cytoskeletal protein that links thin filaments to
the sacrolemma.
o This membrane in turn attaches to the CT matrix that surrounds
muscle fibers. This helps transmit contraction tension to the
tendons.
o Defective types cause muscular dystrophy. Discussed later
Changes During Contraction (the sliding filament
mechanism)
Hanson and Huxley, mid 1950’s proposed this idea.
figure 10.7, p. 282. fig 10.8 p 283
Note in fig 10.7:
1. A relaxed sarcomere showing Z disc, I band, A band, thick
filament, thin filament.
2. A contracted sarcomere showing Z disc, nearly complete overlap
of thick and thin filaments.
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• Remember, this myofibril is only 1 in a muscle fiber so the
effects are additive throughout the muscle.
• During contraction, myosin heads (fig. 10.8) attach, pivot,
and therefore pull on the thin filaments (actin) causing them
to slide toward the H zone (area of only myosin fibers around
M line) at the center of the sarcomere.
o It is a ratcheting type of movement.
o About 1-2 um of movement. This is an additive along the entire
length of the fibril.
o So if you had 100K sarcomeres end to end x 2 (um)
contraction/sarcomere = 200K um in total length contraction.
Convert to cm = 20 cm.
• The sarcomere shortens, but the lengths of the thick and
then filaments do not change. This is the sliding idea.
• The myosin heads ultimately release the thin filament and
allow the sarcomere to relax (return to resting length).
• Shortening of many sarcomeres cause the shortening of the
whole muscle fiber and the entire muscle.
In a contracted sarcomere:
• The A band is unchanged in width.
• The I band is reduced or absent.
o Why? The actin in the I band slid over the myosin toward the M
line.
• The H zone is almost absent. So now we have no area
where myosin is not cross bridged with actin.
There are more details to this mechanism that we will discuss
soon.
Exercise induced muscle damage (DOMS) p.279
• Extensive exercise can cause damage to muscle cells.
o Electron micrographs show torn sarcolemmas, damaged
myofibrils, and disrupted Z discs.
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o Increases of myoglobin (O2 binding protein in muscle tissue),
and 2 enzymes (lactic acid dehydrogenase (LDH)), and
creatine phosphokinase (CPK)) are seen in the blood due to
muscle cell leakage.
• Muscle soreness occurs 12 to 48 hours after strenuous
exercise, called delayed onset muscle soreness (DOMS)
accompanied by stiffness, tenderness, and swelling.
Assignment Question
Describe and illustrate the microscopic structure of skeletal muscle.
Other Structural Components of Skeletal Muscle
All structures mentioned so far have been located within the
sarcoplasm of a muscle fiber.
Other structures within the sarcoplasm include:
Fig. 10.3
• Many mitochondria
o Arranged in rows through out muscle fiber.
o Found close to muscle proteins that use ATP.
o Provides energy (ATP) for contraction using O2, and glucose
or fatty acids.
• Sarcoplasmic reticulum (SR)
o Similar to smooth endoplasmic reticulum in a non muscle
cell.
o It forms a network around each myofibril and functions as a
reservoir for Ca2+ ions.
o Release of Ca2+ ions into the sarcoplasm through calcium
release channels triggers the thick and thin filaments to slide
over one and other and contract the muscle length (more on
this later).
o The Ca2+ provides the final ‘go’ signal for initiating
contraction.
• T (transverse) Tubules
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o Tube or tunnel-like foldings of the sarcolemma that penetrate
inside the muscle fiber.
o The tubules are open to the outside of the cell and contain
ECF.
o These tubules allow a chemical message for contraction (from
a neuron) to penetrate the interior of the myofiber so that all
myofibrils within it can contract simultaneously (more on this
later).
• The SR and the T tubules participate directly in muscle excitation and
lie side by side.
o The T tubules are surrounded by terminal cisterns of the SR
forming a triad appearance.
o Triad = a transverse tubule with a dilated sac of SR called
terminal cisterns of either side.
o There are 2 triads per sarcomere.
Excitation of Skeletal Muscle
p 282-284
How is the skeletal muscle stimulated to contract?
Introduction
Stimulation of skeletal muscle contraction is primarily by
nerve stimulation.
Nerve impulses travel from one part of the body through
nerve cells called neurons.
The connection between 1 neuron and a 2nd neuron (or
neuron to a muscle) is called a synapse.
A look closer at nerve system messages:
• Electrical in nature along the neurons, but are chemical in nature
when crossing a synapse.
• Therefore, nervous system messages are initially electrical followed
by chemical propagation.
Motor Neuron Messages
figure 10.2 p. 277 fig 10.11 p 287
• Two neurons in sequence
o Review the anatomy of a 2 neuron circuit showing with several
axon terminals, a synaptic cleft, a 2nd receiving neuron with
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cell body receiving the chemical message, with extending axon
and axon terminals.
• Sensory neurons take in information to the CNS.
• Motor neurons
Fig 15.8 p 513
send out information away from the CNS.
o The message starts in the CNS in the primary motor cortex.
o The message travels down an upper motor neuron to the spinal
cord were it synapses with a lower motor neuron (or
interneuron).
• Each lower motor neuron has a threadlike axon that travels from the
spinal cord (or lower brain) to a group of skeletal muscles that it
controls. Fig 10.14 p 291
o Each neuron branches profusely near the muscle tissue to as
many as 1000 separate muscle cells (fibers).
Motor Unit p 291
• Each motor neuron and its associated muscle cells = a
motor unit. Figure 10.14 p. 291.
• The number of muscle fibers controlled by a motor unit will
depend on the function of the muscle. Examples:
o A power muscle such as the gluteus maximus or gastrocnemius
will have a motor unit that controls many muscle fibers (about
2000).
o A finesse muscle such as the eye or larynx muscles, will have a
motor unit that controls only a few muscle fibers (about 10-20
eye, 2-3 larynx).
• The average motor unit controls 150 muscle fibers.
• The strength of contraction depends in part on how many
motor units are stimulated.
Neuromuscular junction
Fig. 10.11 p 287, 10.2 p. 277 text p 285
• A synapse is a gap between 2 structures that can only be
crossed by chemical messengers.
• The chemical messengers are called neurotransmitters.
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o Neurotransmitters are stored in membrane-bound vesicles of
the nerve ending (axon terminal), each containing thousands of
neurotransmitter molecules.
o When an impulse moves along the axon and arrives at the axon
terminal, these vesicles migrate to the membrane in the gap
and release their neurotransmitter into the synaptic cleft.
o The neurotransmitter then diffuses across the synapse and
joins to the receptor molecules embedded in the membrane of
the nerve or muscle cell where it stimulates a muscle fiber.
o Each motor end plate typically contains 30-40 million
neurotransmitter receptors.
o Drugs or toxins can affect various neurotransmitters, their
receptors, or reuptake mechanisms found throughout the
nervous system. Examples will be discussed soon.
Diagram of Neuromuscular Junction (NMJ)
This junction is where nerve endings and muscle meet.
The junctions occur near the middle of each muscle fiber.
This allows a stimulus to travel in all directions of the muscle fiber
simultaneously.
Use figure 10.12 p. 288.
Note these features in a drawing of the NMJ 3 stages:
1. Axon terminal (nerve ending) with vesicles containing
neurotransmitter and motor end plate, a specialized area of the
sarcolemma (plasma membrane).
2. A nervous impulse causing vesicles to release
neurotransmitter from the axon terminus with neurotransmitter in
the synaptic cleft area, diffusing towards the motor end plate.
3. The axon terminal at rest and neurotransmitter binding to the
motor end plate.
Neural muscular junction notes
Now we can discuss how the NMJ functions.
Overview of events
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1. At rest, the axon terminal is ready to release neurotransmitter when
an impulse arrives. The synaptic cleft is clear of neurotransmitter.
2. When an impulse (action potential AP) arrives, the vesicles (due to
Ca++ flowing thru the protein voltage gate) move to the axon
terminal and release their neurotransmitter into the synaptic cleft
where it diffuses towards the motor end plate located in the
sarcolemma of a muscle fiber.
3. The neurotransmitter binds to the post synaptic membrane of the
motor end plate. This initiates the continuation of the impulse in the
2nd cell.
Detailed Explanation of the NMJ Physiology
ACh: The NMJ Neurotransmitter
• In the case of a neuromuscular junction, the neurotransmitter =
acetylcholine (ACh).
• Each motor end plate typically contains 30-40 million ACh receptors.
• Each molecule of acetylcholine (ACh) works to change the
permeability of the muscle membrane (sarcolemma) to certain ions
located in the ECF (Na+) and ICF (K+).
Activities of the Membranes in the NMJ
Fig 12.11c p 287
Membrane resting potential
++++++++++++++++
-----------------
membrane fig 12.9 p 397
1. Certain ion concentrations exist on both sides of the
membrane. This condition makes impulse transmission
possible.
a. This is due primarily to:
i. K+ leaks out at 50-100x the rate of Na+ in. So, a voltage gradient is
established at the membrane surface. More negative inside the
membrane suface as K+ moves out to ECF. Proteins (with neg
charge) and PO4- stays behind. This establishes most of the
voltage across the membrane, about -90mV.
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ii. The action of the sodium/potassium pump that pumps 3 Na+ out
and 2 K+ in. This pump uses ATP for energy.
1. However, K+ does not leak back in as fast as Na+ leaks back
out, so a voltage gradient is established.
2. Also, 3 Na+ are pumped out to 2 K+ pumped in so this
contributes to the voltage difference.
2. Therefore, the membrane is said to be polarized = resting
potential.
a. The outside being positive (+) and the inside negative (-), like a tiny
battery.
b. Example: rbc = -10mV, skeletal and heart muscle = -70mV
Membrane Events That Initiate Muscle Activation
1. If enough molecules of ACh bind to receptors sites in high
enough concentration, a depolarization will take place.
2. This is an example of a graded potential where a small area of
membrane (localized at the NMJ) has deviated from the resting
potential.
3. The electrical current flow of Na+ will vary in amount
(amplitude) depending on the strength of the stimulus (amount
of ACh release).
a. The ACh receptors contain Na+ gates that open when binding occurs.
b. The ACh receptor is a channel protein that passes small these
cations (Na+).
4. The depolarization spreads along the membrane in ECF and
cytosol for only a few um before it dies out. So, only good for
short distance communications.
5. When rapid depolarization occurs and spreads across the
muscle cell, it is called an action potential.
Spread of the Action Potential Across the Muscle Fiber
Fig 12.12 p 401
1. When Na ion rushes in at the NMJ, this changes the resting
potential into an action potential that travels locally along the
muscle cell sarcolemma.
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2. The action potential propagates on the muscle cell surface by
triggering other Na+ channels to open that causes the entire
muscle cell to contract simultaneously.
a. These Na+ channels open in response to depolarization in the
membrane near them. So called voltage gated channels.
b. The mechanism of contraction in the muscle cell soon.
Resetting the Resting Membrane Potential
1. One problem is left to be solved: reset the membrane for the
next impulse to be received.
a. We need to get ACh away from receptors sites.
b. If ACh stays, we would get a continual contraction of the muscle cell =
tetanus.
2. To get rid of ACh, the cell has an enzyme called
acetylcholinesterase (AChE).
a. AChE interacts with ACh and breaks it down, therefore removing the
trigger that keeps the receptor Na+ channels open.
b. After the ACh is gone, the permeability of the sarcolemma returns to
normal and therefore, goes back to resting potential, a process called
repolarization.
c. This process will be discussed in more detail when we discuss the
nervous system.
Muscular Disorders or Diseases the Skeletal Muscle
Excitation Mechanism
Myasthenia gravis
box, p.302
• A progressive neural muscular disorder characterized by abnormal
fatigability (weakness and atrophy) of the muscles.
• Muscles are weak, and contract with little force or speed.
• It is an autoimmune disorder that is caused by antibodies directed
against ACh receptors in the motor end plate.
o The antibodies bind to the ACh receptors and hinder the action
of ACh.
o The disease advances as more receptors are affected and the
muscles are weaker and may cease to function.
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• Anticholinesterase drugs (neostigmine) help by making more ACh
available in the synapse to bind to remaining functional receptors.
• Plasmapheresis can be used to remove antibodies from the blood.
Paralysis
• Inability to voluntarily control skeletal muscle. A general term.
• Usually due to nerve damage (denervation - severed nerves), as
muscle will still respond to direct (external) stimulation.
• However, the lesion could be of nerve or muscle origin.
Fatigue
p.290
• If muscle is over stimulated the strength of contractions
becomes progressively weaker to the point where they won't
respond.
• The muscle is in a state of continuous of contraction.
o Example: writers cramp, a temporary contracture.
• It occurs when the muscle cannot release adequate Ca++
from the SR .
• Surprisingly, ATP levels are similar to resting muscle.
• Factors that cause this are:
o Insufficient O2, depletion of CP, depletion of glycogen, build up
of lactic acid and ADP, or ionic imbalance (too much Na+
inside, too much K+ outside), too little ACh in synapse in
response to stimuli (APs).
• So, powerful muscle efforts reach this state quickly, while
lighter effort endurance activities can last for hours in a
person who exercises regularly.
o The question becomes, can the mitochondria keep up with the
level of muscle activity?
Muscular Dystrophies
box, p.302
• Inherited muscle destroying disease, where muscle cells
degenerate and may be replaced with fibrous C.T. or fat.
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o Wheel chair use may be the result at teen years, followed by
death at 20-30.
• Most common is Duchenne M.D., a sex-linked disease of
boys, diagnosed usually from ages 3-5.
o Females are the carriers and transmit the disease to their sons
(1 in 3500 births).
o X chromosome linked; boys only have one X so recessive gene
is expressed in a single dose.
o A protein in the sarcolemma, dystrophin, is missing and seems
to lead to muscle fiber degeneration.
• No treatment is currently available, however gene therapy
(myoblast transfer and plasmid injection) is being
investigated.
Drug Effects on Muscular Excitation
Cholinesterase Inhibitors
• Cholinesterase inhibitors bind to AChE and prevent degrading ACh.
o Examples:
o DFP (a standard organophosphate, diisopropylfluorophosphate)
o parathion (both nerve pesticides)
o sarin nerve gas
o neostigmine (chemical drug used in treating myasthenia
gravis).
• The inhibition of AChE causes spastic paralysis of the muscles, a
state of continual contraction.
o There is an immediate danger of suffocation if laryngeal and
respiratory muscles are affected.
o The poisoned person should remain still and quiet to avoid a
startle response that could escalate into dangerous muscle
spasms.
• Atropine, an ACh antagonist, is given as an antidote treatment for
cholinesterase inhibitors.
o Atropine blocks ACh at post ganglionic cholinergic musarinic
receptors.
o These receptors affect smooth muscle in GI, pulmonary,
exocrine, heart, eye.
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o Used in eye exams to dilate the pupils
Curare
• Causes flaccid paralysis by binding to ACh receptors without causing
stimulation, and blocking ACh action.
• Therefore it blocks the neuromuscular junction.
• Respiratory failure can result.
• Used by South America Indians to poison arrows.
• Historically used to relax muscles in abdominal surgery (abdominal
and diaphragm muscles) so they can be moved aside.
o Now replaced by newer drugs.
Blackwidow spider venom
• Contains many toxins of which one promotes constant release of
neurotransmitter.
• Results in tetanus, a state of constant contraction.
• When the diaphragm muscle is affected, breathing action is ceased.
Botulism
• In botulism, a toxin called botulinum is produced by the bacteria,
Clostridium botulinum. It is ingested with contaminated food.
o This toxin prevents the release of synaptic vesicles containing
ACh, and therefore blocks nerve transmission.
o A type of flaccid paralysis results.
o It is the most potent toxin known: 0.0001 mg will kill a person.
1/2 lb. could kill all humans.
Assign question
What is a motor unit? How does it related to total strength of contraction?
What is a neuromuscular junction? What events occur at the junction?
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The Sliding Filament Theory (1954, Hanson and Huxely)
Overview
P 282-6
• These 2 investigators proposed that skeletal muscle
shortens during contraction because the thin (actin)
filaments slide over the thick (myosin) filaments.
o Then, they would overlap to a greater degree.
• Rather than:
o The previous idea that the filaments change in length themselves, or
possibly fold.
Fig. 10.7 p.282
• In a relaxed muscle the thick and thin filaments overlap
slightly, but during contraction, the thin filaments penetrate
more and more deeply into the central region of the A band.
o The thin filaments pull the Z disc they are attached to toward
the thick filaments which shortens the sarcomere.
o Remember, the I band and the H zones disappear as the thin
filaments move to the center. The A band stays the same
length.
o Only the length of the sarcomere changes, not the length of the
filaments!
• This shortens the whole muscle fiber and ultimately the
whole muscle.
• Their model is known as the sliding filament mechanism of
muscle contraction.
Closer Look at the Events During Contraction
Now take a look at contraction in a step-by-step fashion.
17 steps will be described during a muscle contraction event.
Note:
Figure 10.12, p. 288, explains these events in 9 steps.
It is not important that you can name a step, but that you can explain how muscle
contraction works.
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1. Nerve impulse arrives at neural muscular junction from the
CNS. (The sarcolemma is at a resting potential at this point).
Fig 10.12,1
2. ACh (acetylcholine) release from axon terminals. Fig 10.10,2
3. ACh binds to active sites (protein receptors) on motor end
plate. Fig 10.12,2
4. Development of a graded potential that triggers a muscle action
potential (AP). Fig 10.12 2,3
a. ACh receptor protein channel increases permeability of Na+
into sarcoplasm.
i. A graded potential develops as the chemically gated
receptor/channel opens in response to ACh binding.
ii. This is a localized (a few um), small deviation from the
resting membrane potential.
b. Acetylcholinesterase (AChE) begins to degrade ACh in the
synaptic cleft.
c. If there is enough ACh action to open enough Na+ channels
(that is, enough of a graded potential), an action potential
(AP) will occur.
(Steps 1-4 represent nerve impulse recognition due to a local, graded
potential at the neuromuscular junction.)
5. Na+ enters muscle fiber, depolarization of sarcolemma occurs
= action potential.
a. Voltage changes to a less negative charge across the
sarcolemma.
b. Voltage gated Na+ channels open in response to the
original chemical gated Na+ channels opening.
6. The action potential spreads away from the end plate in all
directions on the sarcolemma as more voltage gates are
triggered and ultimately descends into the T (transverse)
tubules where depolarization continues.
7. When the action potential continues down the T tubules that
penetrate the sarcoplasm, it stimulates voltage sensing
receptor membrane proteins that link with the sarcoplasmic
reticulum (SR) membrane channels for Ca++ release.
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(Steps 5-7 represent depolarization. Fig 10.12, 4)
8. The SR responds (within 1 ms) to the action potential by
opening Ca+2 release channels which floods the surrounding
sarcoplasm located between the thick and thin filaments.
a. Ca+2 flood last about 30ms.
b. A continuously active ATP-dependent pump is pumping
Ca+2 back into the SR.
9. Ca+2 combines with the regulatory protein troponin that is
bound to tropomyosin.
a. Tropomyosin is wound around the actin filaments, blocking
the binding site on actin for myosin when Ca+2 levels are
low.
10. Troponin changes shape, which moves the troponintropomyosin complex deeper into the actin helix structure, and
exposes the myosin binding sites on actin.
See figure 10.9, p. 284, diagram of myosin with heads.
11. Myosin heads can now attach (cross bridge formation) to actin
binding sites on thin filament.
Figure 10.8, 2, p. 283, actin myofilaments and myosin filament with heads attaching to
actin binding sites.
12. Myosin head flexes toward the center of the sarcomere,
pulling actin filaments of sarcomere toward each other (toward
the middle of the sarcomere).
a. This is called the ‘power stroke’ of contraction.
Fig. 10.8 3,4, p. 283, myosin with head in the cocked forward position and then
flexing back onto the myosin filament.
13. Once the myosin head is flexed, ADP is released from the
head and its ATP binding site is exposed.
14. The myosin head detaches from actin binding site under the
influence of ATP binding. Fig 10.8 4
a. This is called ‘cross bridge detachment’.
b. The myosin head has an ATPase activity in the ATP binding
site.
c. ATP is split and transfers energy, ADP, and P group to the
head.
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d. Energy from ATP returns the myosin head to the cocked
forward position.
e. The myosin head is now in its upright, high energy position,
back to where it started.
f. You can now see that the myosin is ‘precharged’ so when an
AP is received, it is ready. This state can be achieved as
long as ATP is available.
g. APs received now will cause the myosin to reattach and
further pull the actin along.
h. This gives the impression of myosin heads ‘walking’ over the
adjacent actin filaments during muscle shortening.
(Steps 11-14 are repeated during a contraction event if ATP and Ca+2 are
available.)
Rigor mortis
box, p. 285
• Notice that ATP is responsible for myosin heads detaching from actin,
which leads to muscle relaxation. In other words, myosin cannot
detach without ATP present.
• This is illustrated by rigor mortis.
o When a person dies, no more ATP is synthesized as no more
02 and glucose are supplied to the tissues.
o The myosin heads cannot detach themselves from actin
resulting in a condition in which muscles are in a state of rigidity
(they cannot contract or stretch) called rigor mortis.
o This state lasts about 24 hours and disappears as the tissues
undergo autolysis. (Lysosomes are broken down and release
their contents.)
15. Ca+2 is returned to the SR by the Ca+2 active transport pump
(requires ATP) and the Ca2+ channels close.
a. Sarcoplasm is now Ca+2 poor.
b. (The Ca+2 is bound to a protein, calsequestrin, in the SR. If
this high concentration of Ca+2 is not bound it would combine
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with PO4- to form hydroxyapatite, as in bone, which would kill
the cell.)
16. Troponin again covers actin binding sites. Therefore no
myosin-actin interaction can occur.
17. Muscle fiber relaxes. Movement of relaxation is due to:
a. "Elastic effect" of coiled elastic fiber (titan) molecules, and/or:
b. Due to pull of C.T. within muscle.
ATP and Contraction
ATP is required for 3 major roles in contraction:
1. Reposition (cocking) of myosin molecule when muscle is
relaxed. Fig 10.8, 1
a. This reaction transfers energy from ATP to the myosin head
even before contraction begins.
b. The myosin heads are in an activated state (cocked and
energized).
2. Detachment of myosin heads from actin once the power
stroke is complete. Fig 10.8, 4
a. Myosin remains flexed and bound to actin until another ATP
molecule binds it. This is the recovery stroke.
b. Each cycle of the head consumes one molecule of ATP. (Some
evidence disputes this.)
3. Powers the Ca+2 active transport pumps that rapidly remove
Ca+2 from the sarcoplasm back into the sarcoplasmic
reticulum. Fig 10.12, 7
a. The concentration of Ca+2 is 10,000 times lower in the
sarcoplasm of a relaxed muscle fiber than inside the SR.
Muscle stores enough ATP for 4-6 seconds of activity.
It is regenerated in 3 ways:
Fig. 10.13, p.2289 text p 289-90
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1. Interaction of ADP with creatine phosphate (CP).
(Phosphagen system)
a. CP is an energy rich small molecule only found in muscle cells,
at 3-5x amount of ATP. Fig 10.13 a
b. When ATP levels drop during work, CP is used to make ATP
quickly.
c. Duration of benefit: ATP + CP will provide muscle power for
about 15 seconds.
i. What can you do in 15 seconds? Run away! Good for a
100m dash! Climb a tree! Attack!
d. Creatine is a popular dietary supplement to enhance muscle
mass among power athletes.
e. Products of reaction: 1 ATP, 1 CP, 1 creatine. CP is built back
up during rest periods.
2. Stored glycogen via the anaerobic glycolysis pathway.
(Glycogen-Lactic Acid System) fig 10.13 b
a. When activity level surpasses the O2 level available for the
mitochondria to use for respiration, this system takes over.
b. Products: 2 ATP per glucose, lactic acid.
c. No oxygen is needed! Called an anaerobic process. Lactic acid
can be used by liver cells, heart muscle, and kidney cells to
make ATP.
d. However, in skeletal muscle, build up of lactic acid lowers pH
and causes pain.
e. Duration of benefit: 30-40 seconds of maximal activity.
Example: 300m race
3.
Aerobic respiration. Fig 10.13c
a. Occurs in mitochondria that are in great numbers in
muscle.
b. The process is slower than glycolysis but yields much
more ATP but requires oxygen.
c. Can burn glycogen (glucose), fatty acids, or protein.
d. Products: 36 ATP per glucose. CO2, H2O given off as
waste. Heat.
e. Duration of benefit: after 30 seconds to hours. Note: to
burn fat, use light to moderate exercise so mitochondria
can keep up with energy needs.
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Oxygen Consumption after Exercise
p 291
Oxygen debt (older term) = recovery oxygen uptake (newer term)
• The amount of oxygen that must be ‘paid back’ to the body following
exercise.
• You know you breather harder, more vigorously after exercise to take
in more O2 and remove CO2. While the body is hotter than normal
and the heart and breathing muscles are working hard, more oxygen
is needed.
o Example: when get out of class early and run to car!
• A 100m dash requires about 6L of O2 for totally aerobic respiration,
however you can only take in about 1.2 L (VO2 max).
o VO2 max is the maximal rate of oxygen consumption by aerobic
respiration. This is largely genetically determined but can be
increased 20% or so by training. Elite athletes have double this
rate.
• So, you develop an O2 debt.
Extra oxygen received during recovery does 3 things:
1. Convert the lactic acid back into glycogen via the liver.
2. Resynthesize creatine phosphate and ATP
3. Replace oxygen removed from myoglobin in the muscle during
exercise.
Physiological Properties of Muscles
• Stimulus = an impulse.
• An impulse may travel along a motor neuron that is not
strong enough to cause a contraction. Fig 12.11 p 399
• Study the graph of electrical potential in millivolts (mV) vs.
time at the membrane surface.
o It should show a range of -70 mV to +40 mV on y axis.
o A stimulus that does not cause a response by the muscle is
called subliminal or subthreshold stimulus.
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o By increasing the stimulus, a barely perceptible response may
be obtained = liminal or threshold response.
o It is just strong enough to cause a depolarization and
production of an action potential. Action potentials trigger
contraction.
o This is a change from –70mV to –55mV at the membrane
surface.
o A maximal response is one in which all the fibers of the muscle
are active.
Assign questions
What is the sliding filament mechanism? Describe the role of calcium and regulator
proteins in the sliding of filaments.
What changes permit a muscle fiber to relax after contraction?
Grading of Strength of a Contraction
or How can we control how much strength a muscle produces?
• An individual motor unit fires all muscle fibers in that unit in an ‘all or
none’ fashion.
• All fibers contract to there fullest extent.
The whole muscle tension however can be adjusted.
There are 2 ways to control strength of a contraction:
1.
2.
Recruitment of motor units.
Altering the contractility of individual muscle fibers.
1. Recruitment of motor units. (multiple motor unit summation) p. 292
An individual neuron branches to many different muscle fibers. The
neuron and the muscle fibers it activates are together called = motor
unit.
a. Motor units vary in size
b. A small motor unit may consist of as few as 10 fibers, while a large
one may consist of several 100.
i. Example: Fingers contain very small motor units so they can carry
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out fine movement.
c. Simply speaking: If a muscle needs more force, it will recruit (activate)
more motor units. If not so much force is necessary, less are
recruited.
d. The strength of the electrical stimulus determines the amount of motor
units recruited.
i. Threshold stimulus causes the first observable muscle contraction.
1. A threshold stimulus recruits the most excitable motor neurons
first that control the smallest motor units.
2. Example: the hand is used to lightly pat a cheek
ii. Maximal stimulus is the strongest stimulus that still causes
increased contraction.
1. A maximal stimulus recruits the strongest contraction possible
by recruiting the larger motor units driven by less excitable
neurons.
2. Example: a sharp slap to the face
iii. The primary function of motor unit recruitment is create smooth
movements not just more contractile force.
1. We demonstrated this in lab the first night with the stimulator, a
transition from jerky contraction to a smooth maximal
contraction.
2. Experience is important in knowing how many motor units to
recruit.
a. Other wise you could hurt yourself or damage something.
b. Example: I
i. If you pick up a milk carton that you thought was full and is
empty you will probably spill some milk.
ii. So, when you pick something up that you think is heavy
but is an illusion, you will recruit too many motor units
and the muscle will over react.
iii. Can you think of examples where you have done this?
iv. A young child with a small pet?
3. Motor units usually contract asynchronously in that some motor
units are in tetany and some are relaxed. This prevents or
delays fatigue.
2. Altering the contractility of individual muscle fibers.
This means changing the properties of muscle fibers irrespective
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of how many fibers are involved.
There are 2 ways to change the contractility of fibers.
1. Increase the frequency of stimulation to individual fibers.
2. Vary the length of the fiber (length-tension relationships).
1. Increasing frequency of stimulation.
• First, let’s see how we can hook a muscle up to the following
apparatus and measure changes in force:
o Draw a frog muscle anchored at one end, and anchored to a
force tension transducer at the other end. Show the transducer
wired to a physiograph that has a paper recorder.
o Keeping the muscle at a fixed length and stimulating it, we can
measure a change in tension overtime:
• A single muscle twitch
Figure 10.15 p. 292.
o Draw a myogram showing a single isometric twitch, with tension
on the Y axis and time on the X axis.
o The tension produced from the stimulation is called a twitch,
because it takes place when the muscle length is fixed.
o It is called an isometric twitch = tension but no shortening.
o As opposed to isotonic twitch = tension and shortening.
• Summation effect or wave summation of 2 or 3 stimuli
o If 1 stimulation quickly by another, you see what is called the
summation effect or wave summation = the tension produced
in the second stimulation will be added to the first, that is it will
be stronger. Figure 10.16b page 293.
See the myogram with tension on the Y axis and time on
the X axis. The first stimulation, S1 is to the right followed
by the second stimulation, S2 near the peak of the first
contraction.
o This occurs because the cell membrane has repolarized (takes
about 5 ms) but the muscle sarcomeres have not completely
relaxed (are partially contracted because it takes time to pump
Ca+2 back into SR) (takes 10 –100 ms) and more calcium is
released that adds to some of that released in the first stimulus.
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However, summation is not an infinite effect which leads us to tetanus.
• Complete (fused) and incomplete (unfused) tetanus
o If there is repeated stimulation, tension will reach a certain
plateau and stay there (this is known as tetanus).
o Neurons normally deliver nerve impulses in volleys, not single
impulses as we demonstrate in class.
o This is how we have smooth and sustained muscle activity.
Figure 10.16d, p. 293.
See the myogram demonstrating complete (repeated fast
stimulations, 80-100/sec) and incomplete tetanus
(repeated slow stimulations, 20-30/ sec).
•
•
•
•
Incomplete (unfused) tetanus fig 10.16c
Muscle can only partially relax between stimuli.
Occurs at 20-30 stimuli/sec.
Complete (fused) tetanus
o Muscle has a sustained, smooth contraction with no relaxation.
o Occurs at 80-100 stimuli/sec.
o This is how muscle stimulation usually occurs with volleys of
stimuli in rapid succession from the neurons (CNS).
o The tension (strength) is 2-4 times the tension of a single
twitch.
o Eventually, the muscle will run out of ATP and will fatigue (force
will go to zero).
Another way to alter the contractility of a fiber:
2. Vary the length of the fiber (length-tension relationship)
•
% Sarcomere length vs. tension
p285
o If we examined this at the magnification level of the myofibril,
we could plot sarcomere length vs. tension. Figure 10.10. p.285
o Draw a myogram with tension on the Y axis and sarcomere
length in um on x axis from short to long.
o Maximum tension occurs at about 2.2 um.
o This is the ‘sweet spot’ for fiber overlap and strength.
• What is the reason for this? Let's look at a sarcomere at the different
lengths.
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o View the sarcomere at 2.1 um and at 3.8 um length. Figure 10.10.
See that the more contracted the sarcomere, the greater
the overlap between thick and thin filaments.
The more they overlap, the more cross bridges which can
connect and hence, more tension can be produced.
But thick filaments crumple as they are compressed by
the Z discs when sarcomere shortening is extreme.
The thick and thin filaments interfere with each other and
break myosin bonds.
o If the sarcomere is stretched so that the thick and thin filaments
cannot overlap very much, contraction decreases.
o If stretched to about 175% of optimal length, no myosin heads
can crosslink with thin filaments, and no contraction can occur.
o In the body, resting muscle fiber length is maintained at 70130% of the optimum, because of the way muscles are
anchored to bones and C.T.
Types Of Skeletal Muscle Contractions
Fig. 10.17 p294
Isotonic Contractions: the contraction of movement
• Tension is produced and overall shortening of the muscle occurs as a
load is moved through the range of motion to the joint .
• Example: These contractions draw two bones together and serve to
bring about movement.
o (concentric contraction: muscle shortens during contraction fig
10.17a
o (eccentric contraction: muscle lengthens during contraction fig
10.17b
o These 2 types together bring about coordinated, smooth
movements.
Isometric Contractions: the contraction of stabilization. Fig 10.17c
• Tension is produced but no shortening of the muscle occurs.
• Energy is still used! Crosslinking occurs but no sliding of filaments.
o Example: These contractions serve to keep the body fixed in
position as in maintaining posture. As in the neck, trunk, legs,
feet.
• Most body activities involve both isotonic and isometric contractions.
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Twitch
A single isotonic response as a result of a brief threshold
(liminal) stimulus.
• (This is not the type of twitch you feel in your body due to being tired
or a chemical imbalance).
• The muscle contracts quickly and then relaxes.
• A twitch can be demonstrated by an instrument that produces a
myogram, a tracing of a muscle contraction.
A simple muscle twitch consists of 3 phases, they are:
Fig. 10.15, p.292
1. 1.Latent Period
a. The time from stimulation of the muscle until shortening of the muscle
begins. The latent period is a “lag time”.
b. Duration = about 2 ms.
c. During this period of time the following events of muscle contraction
are occurring:
i. Depolarization, action potential triggered (1-2 ms), repolarization
begins.
ii. Diffusion of Ca+2
iii. Establishment of actin/myosin bonding
d. Uptake of elastic connective tissue in muscle to bone connection.
2. Contraction Phase
a. Tension and shortening of the muscle occurs.
b. The upward tracing represents this phase.
c. Repolarization is completed and refractory (non excitable) period ends
(within 5 ms).
d. Duration = 10-100 ms.
3. Relaxation Phase
a. Muscle goes back to it resting state.
b. The downward tracing represents this phase.
c. The Ca+2 is actively transported back into the SR which results in
relaxation.
d. The sarcomere begins to recoil back to resting length.
e. Duration = 10-100 ms.
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Types of Muscle Skeletal Muscle Fibers
table 10.2 p.296
In humans we see 3 types of skeletal muscle fibers classified on 2 factors:
1. How fast the muscle will twitch, and
2. Method of ATP generation.
1. How fast a muscle will twitch (due to how fast myosin head ATPase
splits ATP). Factors:
a. How much myoglobin is in the muscle fiber.
i. Myoglobin is a respiratory pigment that binds O2 for ATP
generation.
ii. It makes muscle appear red.
iii. If absent, then fiber appears white.
b. Number of mitochondria available
i. The more available, the more sustained level of activity.
ii. Number of capillaries that serve the muscle fiber.
iii. The more capillaries available, the more nutrients and wastes can
be transported.
2. Metabolic way used to generate ATP. Review fig. 10.13
a. Respiration uses O2 and occurs in the mitochondria = oxidative
metabolism.
b. Fermentation occurs when O2 is not available = anaerobic
metabolism.
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Table of Characteristics of Skeletal Muscle Types
Postural
Walking
Quick Power Moves
Structural Features
Slow Oxidative SO Fast Oxidative FOG Fast Glycolytic FG
Diameter or Fiber
Color/Myoglobin
Mitochondria
Smallest
Red/large
Many
Functional Features
Slow Oxidative
ATP Production
Aerobic (O2)
ATP use/Veloc. of Contrac. Slow
Resists Fatigue
High
Glycogen Stores
Low
Order of recruitment
1st
Intermediate
Red-pink/large
Many
Largest
White/small
Few
Fast Oxidative Fast Glycolytic
Aerobic (O2) Anaerobic glycolysis
Fast
Fast
Intermediate
Low
Intermediate
High
2nd
3rd
Activities/Function/Location:
Slow Oxidative SO:
• Slow twitch, type I, fatigue resistant fibers
• Maintain posture (anti-gravity muscles), endurance running.
• Location: Back and neck muscles.
Fast Oxidative FOG:
• Fast twitch A, type IIA, fatigue resistant fibers
• Walking, sprinting.
• Location: Leg muscles.
Fast Glycolytic FG:
• Fast twitch B, type IIB, fatigable fibers
• Rapid, intense movements of short duration. Ball throwing, weight
lifting.
• Location: Arm muscles.
Other animals use of muscle cell types
Concentrations of fast and slow twitch muscles can be observed in other
animals as well as humans.
• The light and dark meat of a chicken has to do with concentrations of
different types of muscle fibers.
o A chicken uses it’s breast muscle (white meat) for short flight if
at all = fast twitch. The legs (dark meat) of a chicken serve for
endurance = (slow twitch).
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o What type of meat would you expect to find in the breast of a
migratory duck? Dark meat = slow twitch for endurance.
Implications of fast twitch and slow twitch muscles in sports:
• The proportion of slow twitch versus fast twitch muscles you possess
is genetically determined and cannot be changed dramatically.
• In other words training and conditioning can do some change.
Endurance training can change FG fibers to FOG fibers. Power lifting
will increase size and strength of FG due to increase in fiber size and
strength.
o Example:
o Alberto Salazar (marathon runner): 92% red slow twitch, 8%
white fast twitch.
• Sprinters contain about 60% fast oxidative.
• Weight lifters have about equal amounts fast glycolytic and slow
oxidative
• Determination of muscle fiber ratios can be done by muscle biopsy.
See transverse sec., p.296.
Anabolic Steroid abuse
• Testosterone (found in men) and growth hormone influence muscle
growth.
• Anabolic steroid drugs are testosterone like and are abused by
athletes to increase strength and endurance.
o Problems: liver cancer, kidney cancer, heart disease,
aggressive behavior, mood swings.
Females: sterility, facial hair, deep voice, atrophy of
breast and uterus, menstrual irregularities.
Males: testes atrophy, less sperm production, baldness.
Frequency of Stimulation
• Tetanus
o The sustained contraction of a muscle due to increased
frequency of stimulation.
o The result of summation of twitches. Fig. 10.16d p.293
o Tetany results from the summation of twitches and the amount
of force generated is 2-4 times the force of a single twitch.
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o When the frequency of the stimulation is such that there is no
hint of reduced tension or force between stimuli, it is called
complete tetany or fused tetany. 80-100 stim/sec
o When the frequency of stimulation is reduced slightly, you can
see partial muscle relaxation occurring between contractions,
this is called incomplete tetany or unfused tetany. 20-30
stim/sec
o Incomplete tetany can result in trembling (shaky) movements of
the limbs observed in some individuals.
o Normal muscle contractions with smooth movement are a result
of complete tetanic contractions.
Treppe (no longer in Tortora)
Is the increased strength of contraction as a muscle ‘warms up’ due to
identical stimuli too far apart for wave summation to occur.
It is also known as the ‘staircase effect’, as the muscle steps up its strength
with each contraction.
Draw diagram of treppe with identical stimuli too far apart for summation.
(No diagram in Tortora)
Treppe can be explained as follows:
1. A progressive buildup of Ca2+ in the sarcoplasm probably accumulates
because the stimuli release Ca2+ faster than the Ca2+ pump can move
them back in to the SR.
a. The troponin becomes saturated for maximum binding to myosin
heads.
b. Eventually the inflow and outflow of calcium ions equalize and the
strength of contraction will level off
2. In your warming muscles, the sarcoplasm becomes also becomes less
viscous with more heat and the internal resistance of the muscle is
lessened allowing more energy to be directed to muscle shortening and
less to overcome resistance.
a. With increased heat, the enzyme systems become more efficient.
b. This is the basis for the warm-up period for athletes.
Muscle Tone
Physiology 7
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38
• Tone is a sustained partial state of contraction in the muscle.
• They are involuntary spinal reflexes responses to activation of stretch
receptors in muscles and tendons.
• Movements are not produced.
• Tone is maintained in the body without fatigue by the alternation of
different motor units. It serves to keep the body in a state of
readiness for activity at all times.
Hypotonia see box p.302
• Refers to decreased or lost muscle tone, resulting in flaccid
(flattened) shape.
Atrophy see p.279
• Wasting of muscle tissue where muscle fibers decrease in size as
myofibrils are lost.
Hypertrophy see p.279
• Opposite of atrophy.
• Refers to an increase in diameter of muscle fibers where myofibrils,
mitochondria, and SR are increased. Capillaries servicing muscle
fibers are increased too. No increase in # of cells.
• Due to forceful, repetitive strength training, which results in increased
capacity for forceful contractions.
Muscle tone can be lost quickly.
See p.279.
• If muscle usage is prevented by a cast (disuse atrophy), or by a
severing of the nerves (denervation atrophy), the muscle fibers begin
to atrophy in just a few days.
• Muscle ¼ size in 6 – 48 mos. of disuse.
• Prolonged inactivity can lead to degeneration of the muscle fibers and
they may be replaced by C.T., including fat, which cannot be
reversed when complete.
• Direct stimulation of the inactive muscle using a muscle stimulator
may prevent atrophy until the muscle is removed from the cast or the
severed nerve fibers can remake connections.
• The important thing to realize is that muscle health is maintained in
part by utilization - “use it, or lose it!”
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Smooth Muscle
table 10.2, 300
Introduction
• Smooth muscle is also called involuntary muscle (under ANS
control) and nonstriated muscle (lacks organized
sarcomeres).
o Actin and myosin myofilaments are present but are not
regularly arranged leading to the absence of light and dark
bands that cause the striations in skeletal muscle tissue.
Fig10.19
•
Smooth muscle cells have a sarcolemma but contain fewer
myofibrils than skeletal muscle.
• Contractions start slowly and last a relatively long time.
• Maintains steady pressure in GI tract and blood vessels.
Characteristics of smooth muscle in comparison to skeletal
muscle table 10.2
Smooth muscle has:
1. 7 times less actin & myosin in smooth muscle than skeletal muscle with
no sarcomeres.
2. Lower levels of ATP (& creatinine phosphate)
3. Fewer number of mitochondria with slow contractions.
4. Smooth muscle cells lack T-tubules. Slower onset of contraction.
5. Have poorly developed sarcoplasmic reticulum. Takes Ca2+ longer to
diffuse. Some Ca2+ leaks in from ECF. Also delays in sequestering Ca2+
for longer contraction.
6. Contraction regulated by not only neurotransmitters (ACh, NE by ANS),
but also by: hormones, local chemical changes (pH, O2, CO2), and
stretching.
So smooth muscle is designed for slow reacting, but prolonged
contractions.
Note: The two types of smooth muscle will not be discussed.
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Abnormal Contractions Of Muscle Tissue
Spasm p 302
• A sudden involuntary muscle twitch (contraction of short duration),
usually due to a chemical imbalance.
Cramp p 302
• A sustained, painful, spasmodic (tetanic) contraction of a muscle.
• Can last more minutes to hours.
• Severe cramps usually occur when the muscle is shortened (when
there is little pull on the tendons).
• Usually occurs at night or after exercise.
• May reflect low blood sugar, electrolyte depletion (Na+ or Ca+2), or
dehydration. Sensory impulses then trigger a reflex in the spinal cord
neurons to initiate contraction.
• It is not known what actually happens at the level of a sarcomere
during a cramp. However, the pull on the tendons of muscles are
constantly monitored by sense organs called golgi tendon organs. p.
506 fig 15.4
o Golgi tendon organs act to inhibit or “apply the brakes” to
muscular contraction to prevent the development of too great of
tensile force that could result in injury to the muscle or tendon.
o Learning how to keep the golgi tendon organs from working
may be an important part of strength training.
o Maximal vigorous contractions when the muscle is in a
shortened position seems to increase the probability of
cramping.
• How can you relieve cramps in light of this information?
o Simply forcing the muscle into its longest position (stretching)
will create tension on the golgi tendon organ.
o The inhibition caused by the golgi tendon organ will then stop
the cramp.
Convulsions
• Violent, involuntary contractions of whole groups of muscles.
• Convulsions occur when motor neurons are stimulated by factors
such as fever, poisons, hysteria, and changes in body chemistry due
to drug withdrawals.
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• The stimulated neurons send seemingly senseless impulses to the
muscle fibers.
• This is a nervous disorder not a muscular disorder.
Fibrillation p 302
• Uncoordinated contraction of individual muscle fibers so that the
muscle fails to contract smoothly.
• Cardiac muscle is most prone to this type of activity and is recorded
by electromyography.
Assign question
What is a myogram? Describe the latent period, contraction period, and relaxation
period of a muscle twitch contraction.
Distinguish between tetanus incomplete, complete tetanus, and the staircase effect.
Contrast the structure and function of slow oxidative, fast oxidative, and fast glycolytic skeletal muscle.
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Introduction To The Nervous System
Chapter 12 p386 fig 12.1
The nervous system in conjunction with the endocrine system is
responsible for coordination of all of the other human body
systems.
The nervous system is a ‘wired’ system with discrete pathways
and local actions. The effects of nervous stimulation are usually
immediate and short lived.
Example: muscle movement
The endocrine system is specialized to control activities that
require duration not speed.
Hormones are secreted into the bloodstream and have wide
ranging effects on target cells that contain hormone receptors.
Examples: growth patterns, reproduction cycles, metabolism
(glucose), water balance
Functions of the Nervous System:
Fig 12.2 p 388
1. Sensory: afferent neurons
a. Millions of sensory (efferent) receptors monitor changes both
inside and outside the body.
b. The changes are called stimuli and the information gathered
sensory input.
i. Examples: Internal: stretching of stomach, pH changes in
blood.
ii. External: Smells, sights, sounds, pressure, pain.
2. Integration: interneurons
a. It analyzes sensory inputs, stores some information, and makes
decisions about what should be done each moment.
3. Motor: efferent neurons
a. It may cause a response by activating effector organs: muscles
to contract and glands to secrete.
b. This response would be called motor output.
4. Conceptual thought
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a. Capacity to record, store, and relate information received and
use it at a later date.
b. A high level of self awareness.
c. The human brain represents the peak of development of animal
brains.
d. This trend has enabled such adaptive capacities as learning,
introspection, planning, speech and language.
e. Indeed a single humans art, speech and ideas, and deeds may
affect literally millions of other humans, and maybe the
biosphere itself.
Classification of the Nervous System
It is very important that you understand which divisions of the
nervous system are anatomical structures (i.e. a structure you
would actually see during the course of a dissection or operation)
and which nervous system terms are based on function that is,
how it works.
The next 2 diagrams are in your course outline.
Anatomical Classification of the Nervous system
Fig. 12.1, p387
Nervous System
Central Nervous System
1. Brain
2. Spinal Cord
Peripheral Nervous System
1. Nerves
2. Ganglia
3. Sensory Receptors
From an anatomical perspective the nervous system has 2 major divisions:
1. The Central Nervous System.
2. The Peripheral Nervous System.
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The Central Nervous system consists of the brain and the spinal cord and
nothing else!
Any other nervous system structure that connects to the brain or spinal
cord would be a part of
the Peripheral nervous system.
The 3 major components of the peripheral nervous system are:
1. Nerves
2. Ganglia
3. Sensory receptors
1. Nerves
fig 13.10 p. 434
a. Simply defined a nerve is a bundle of neurons or nerve cells.
b. They can be motor, sensory or mixed.
c. 2 important categories of nerves that are a part of the peripheral
nervous system:
i. Cranial nerves (12 pr.) that branch to and from the brain.
1. You need to know these for exam 2. See the detail in the
course outline.
2. For each nerve, know number, name, functions: sensory or
motor or both. These are discussed in table 14.3 p. 485-489 of chapter
14.
ii. Spinal nerves (31 pr.) that exit the spinal cord bilaterally from
between each vertebrae. Fig 13.2 p 422 Discussed on 433-435 fig
13.11.
2. Ganglia fig 13.3 p424
a. Ganglia are aggregations of nerve cell bodies. Ex. Dorsal root
ganglia.
3. Sensory
receptors
fig 15.1 p500
a. Sensory receptors or sense organs as they are sometimes called
serve to give the body information about the immediate environment,
both internal and external.
b. They include the special sense organs involved in your sense of taste,
touch, sight, hearing, or smell.
Functional Classification of the Nervous System
Fig 12.2 p388 Note: we will not discuss the Enteric Motor Neurons(ENS) classification.
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Nervous System
CNS integration
Afferent (Sensory)
Efferent (Motor)
Autonomic
Sympathetic (Stress)
Somatic
Parasympathetic (Calm)
Afferent Division
• The Afferent division of the nervous system is responsible for carrying
information toward the brain.
• The afferent division is also called the Sensory division as it picks up
information about the environment and takes that information to the
brain (CNS).
Efferent Division
• The Efferent division of the nervous system is responsible for carrying
information out and away from the brain.
• The Efferent division is also called the motor division. We will
consider in this class the Enteric Nervous System (ENS) to be part of
the Autonomic nervous system (ANS)
The Efferent division is further divided into 2 parts based on
whether the information coming from the brain is under voluntary
or involuntary control.
1. Somatic Nervous System
• The somatic portion of the efferent division is under voluntary control
and is composed of somatic motor nerve fibers.
• It is the part of the nervous system that serves to innervate skeletal
muscle tissue.
• We have already discussed how you have voluntary control over
skeletal muscle actions.
2. Autonomic Nervous System (ANS)
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46
• You do not have control over the information that passes through the
ANS. For that reason the Autonomic nervous system is sometimes
referred to as the automatic or involuntary division.
• The specific tissues that are innervated by visceral motor nerves of
the autonomic nervous system are:
o Smooth muscle, cardiac muscle, and glands.
Let’s discuss the 2 divisions of the ANS:
a. The Sympathetic division.
b. The Parasympathetic division.
Parasympathetic Division
• The parasympathetic division attempts to conserve body resources.
Restore after exertion.
• It is primarily dominant under calm conditions- ‘rest and digest’.
• SLUDD= salivation, lacrimation, urination, digestion, defecation. The
3 Decreases: heart rate, diameter of airway, diameter of pupils.
Sympathetic Division
• The sympathetic division dominates under conditions of stress.
• It serves to prepare for the quick utilization of body resources.
• The sympathetic division is said to be the division that prepares you
for “fight or flight”.
o Supports vigorous physical activity and ATP production.
o E situations: exercise, excitement, emergency, embarrassment.
Aided by hormone (E and NE) release from adrenal medulla.
• Dilates eyes, increases heart rate and contractions, increase BP,
dilate airway, increase blood to skeletal and cardiac muscle, liver, fat
tissue, glycogenolysis, lipolysis, digestion inhibited. Table 17.4 p 580-1
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This is the handout on the PNS and Cranial nerves. See course outiline.
Peripheral Nervous System (PNS)
The components of the PNS include (1) nerves, (2) ganglia, and (3)
receptors.
Cranial Nerves chapter 14 p 477 table 14.3 p 485-489
Twelve pair of cranial nerves branch from the human brain.
For each cranial nerve you must know the Roman numeral, name, whether
it is sensory (S) or motor (M) or both (B)(mixed), and function.
I
II
III
IV
V
VI
VII
Name
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducent
Facial
S, M or B
S
S
M
M
B
M
B
Function
smell
vision
eye muscles
eye muscles
S - face, teeth & scalp, M - facial muscles
eye muscles
S - taste & tongue, M - pharyngeal muscles
(swallowing)
VIII Vestibulocochlear S
(Auditory)
IX
Glossopharyngeal B
S - taste & tongue, general sensation of pharynx
X
M - pharyngeal muscles (swallowing)
S - visceral sensation
Vagus
B
hearing & equilibrium
M - visceral movement including phonation by
larynx (speech)
*great distribution leads to many visceral functions
XI
Accessory
M
swallowing, head and shoulder movement
XII
Hypoglossal
M
tongue - speech & swallowing
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Electrical Properties of Cells
Electrical potential
If you were to stick an electrode into any cell of the body and compare it to
the outside of the cell you would be able to measure an electrical potential.
ECF ++++
Volt meter
- 70 mV
ICF -----
fig. 12.9 p 397
This electrical potential is produced by differences in concentration of ions
(ion imbalance) on either side of the cell membrane.
Although many different ions are found in the ECF and ICF, the resting
potential is determined mainly by 2 cations: K+ and Na+. More on this later.
The lipid bilayer acts as an effective insulator.
Your textbook calls this a membrane potential.
The electrical potential may be measured in voltage.
Current (I) = voltage(V)/resistance (R) I = V/R: this is Ohm’s law.
Or V= I x R
• Current = the movement of ions across the membrane.
• Resistance = the cell membrane resisting the movement of ions.
• Voltage is the potential energy between the interaction of the ion flow
through the cell membrane.
A greater difference between positive outside ions and negative inside ions
will create more potential current flow (more voltage).
If the membrane resistance to ion flow is lowered, more current will flow.
If the positive and negative ions are in balance on each side of the
membrane, the voltage is zero (0).
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Since such small amounts of electricity are involved the voltage is
measured in millivolts = 1/1000th of a volt.
By convention, the voltage inside the cell (intracellular fluid ICF) is
compared to the voltage out the cell (extracellular fluid ECF).
Fig. 12.10 p.398
• At rest there are more positive ions just outside the cell membrane
than inside so the resting potential of the cell is given as negative
voltage ( average -70 mV, range –40 to –90 mV).
Mechanisms of Establishing Membrane Potentials
There are 2 basic processes that may lead to unequal distribution of
charges ( charge gradient, ion imbalance) on either side of the cell
membrane:
1. Differential permeability of membranes to specific ions.
2. Active transport (Na+/K+ pump).
1. Differential Permeability of Membrane.
• The leakage occurs through protein channels along the membrane
that are always open.
o Therefore they are called leakage or nongated ion channels.
o The major cations involved here are sodium (Na+) and
potassium (K+).
• The cell membrane has more K+ than Na+ leakage channels and is
therefore more permeable to K+ than Na+.
o Permeability of K+ is 50 -100x > Na+.
o Therefore, Na+ ions are found primarily outside the cell.
o K+ ions are found primarily inside the cell but tend to leak out
due to diffusion through the “leaky” membrane.
o It is due to the leakiness of the K+ ions that the inside of the cell
membrane is less positive and said to be slightly negative.
• Note that the large anionic proteins cannot leave the cell and
contribute to the negative charge at the inner membrane.
Fig. 12.9, p.397
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Na+
positive outside
++++++++
-----------Less positive inside
Or
‘negative’ side
K+
Cell
Cell
• K+ ions can’t leak out forever. K+ ions flow down their concentration
(chemical) gradient, outside the cell.
• But the increasingly negative charge (electrical) difference starts to
pull K+ back into the cell and a balance is reached at about –90mV.
o This is called the potassium equilibrium potential.
o Note that K+ moves down its concentration gradient but against
its electrical gradient.
o Since the outside ECF membrane is positive, the K+ ions are
repelled.
• The majority of the resting membrane potential is due to potassium
leakage.
• By itself, the membrane potential would be about –90 mV.
• The resting membrane is modified to about –70mV as Na+ ions flow
across the membrane at slower rates in the opposite direction and
the Na/K pump expels more Na ions than K ions are move inside (3:2
ratio).
• Even though the Na+ leakage is slow, there is no gradient to oppose
it (electrical or chemical), and it would destroy the electrochemical
gradient.
o Note that the Na+ ions move down a chemical and electrical
gradient.
o The inside ICF membrane is negative so the Na+ ions are
attracted.
• Now, there must be a way to establish the high Na+ in the ECF and
the high K+ in the ICF that allows for this membrane potential to be
established.
2. Active Transport: the Na+/K+/ATPase pump.
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There are many active transport pumps in the membrane that move K+ and
Na+ against their chemical gradients.
ATP is expended to create these concentration gradients.
Fig. 3.11 p. 70.
• The Na+/K+ pump serves to move K+ ions into the cell and to pump
Na+ ions out of the cell.
o It requires ATP to configure the protein to act as a pump.
o For every 3 Na+ ions moved out, 2 K+ ions are moved in.
• Since K+ diffuses out of the cell easily, the net effect of the pump is to
remove Na+ from the cell.
• There are 100’s of these pumps per um2 of cell surface.
• The combination of the passive forces of diffusion through a
semipermeable membrane (leaky channels) and the active force of
active transport Na+/K+ pump), there is an unequal distribution of
ions leading to a membrane potential.
• This type of membrane potential is called a resting potential as the
nerve cell is at rest. It remains this way as long as there is no
stimulation.
The membrane is said to be polarized.
ECF
+++++++++++++++++++++++++++++
Cell
---------------------------------------------------------------------------------------------
ECF
+++++++++++++++++++++++++++++
Resting nerve cell or fiber, with a polarized membrane.
As a side note, the primary task of the Na/K pump is to control water concentration in
animal cells. As proteins and other biomolecules are manufactured inside the cell, the
cell may become hypertonic. As a result, water will enter the cell.
In animal cells with no cell wall to protect against the cell bursting as water moves in by
osmosis, Na is pumped out and the water will follow. Remember that the cell membrane
does not allow much Na to enter back into the cell while K can move quickly back out
through membrane channels that are normally open.
Nerve Impulse and Action Potential
Now, we will compare the resting nerve cell with a stimulated nerve cell.
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Action Potential (AP)- the action potential will be described in 2
steps:
Step 1.
The cell membrane becomes highly permeable to Na+ and depolarizes.
Fig. 12.12,steps 1-2 p.401
• When the membrane is stimulated (during nerve excitation) it
becomes highly permeable to Na+.
• Na+ rushes into the nerve cell due to the concentration gradient and
the membrane is depolarized leading to an action potential.
• Na+ enters the nerve cell membrane through special ion channel
proteins called a chemical gated channel.
o When the neurotransmitter (chemical) binds to the membrane,
it opens the ‘gate’ of the protein so Na+ ions can rush in to the
cell.
o This is the graded potential we previously discussed with
muscle excitation. Fig. 12.14, p.405
o The Na+ rushes in due to the concentration gradient (higher to
lower) and chemical gradient (opposites attract, the negative
inside attracts the positive outside).
Voltage Gated Channels
• If enough Na+ enter to a threshold level (about –55 mV), then Na++
voltage gated ion channels in the membrane open to let Na+ rush in
to further depolarize the membrane until it reverses to become +30
mV.
o Electrical protein gates in the membrane are very sensitive to
potential changes and distortions occur that flips them to
another conformation, in this case open.
o Na+ permeability is now 600x greater than K+.
• As a result, further depolarization occurs opening more and more Na+
gates in a positive feedback cycle.
Na Na Na
+
+ + +++++++++++++++++++++
-+--+-- +----------------------------------------------------------------------------------
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+++++++++++++++++++++++++++++
Stimulated nerve cell or fiber, with a depolarized membrane. (Step 1)
Step 2
Resting potential is restored = repolarization.
Fig. 12.12 step 3-4.
The same depolarizing event that opens the Na+ gates also triggers 2
other events:
1. The Na+ gates are triggered to close, after a few 10,000th of a second
after they open.
About 20K Na+ flow thru the gate when open.
2. Voltage gated K+ channels are triggered to a delayed opening, about the
time that the Na+ gates close.
• At this time voltage gated K+ channels are opened that allows
increased diffusion of K+ out of the cell.
• The Na/K pump fine tunes the resting potential disrupted by the
action potential.
• These events allow for the repolarization of the nerve cell membrane
to the resting potential (-70 mV).
K
+
K
+
K
+ +++++++++++++++++++++
-+--+-- +----------------------------------------------------------------------------------
+++++++++++++++++++++++++++++
Resting potential of nerve cell or fiber restored = repolarization. (Step 2)
Each of these 2 events occurs sequentially along the nerve fiber = nerve
impulse.
The relative amount of Na/K that moves across the membrane during an
AP is inconsequential to the ECF/ICF concentrations of Na/K.
So, the concentration gradients are not disturbed, so repeated APs can
occur as soon as the membrane is repolarized.
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Propagation of Action Potential
Fig. 12.13a p.403
The movement of the nerve impulse along the nerve fiber is called
propagation.
• The Na+ ion rushing in moves sequentially in the direction of fewer +
ions along the nerve fiber causing depolarization along the way.
o This is a domino type of effect.
• This propagation along the fiber is called an impulse or conduction.
• Impulses travel from the trigger zone at the nerve cell body (axon
hillock) to the axon terminals toward the next nerve cell or effector
cell (muscle or gland).
o Movement is in one direction because the membrane has
repolarized as soon as it passes as we previously discussed.
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Graphic View of an Action Potential (Impulse)
Let’s review a graphical representation of an action potential.
Fig. 12.11, p.399.
membrane
potential
mV
50
40
30
20
10
0
-10
-20
-30
-40
-50
-60
-70
-80
Depolarization
graded
potential
repolarization
Na+ in
K+ out
threshold for AP (-50-55 mV)
resting potential (-70 mV)
step1
Stimulus
step 2
Time (ms)
hyperpolarization
Effects of Chemicals and Drugs on Nerve Cell Membranes
DDT (dichloro-diphenyl-trichloroethane)
One of the reasons the pesticide DDT is so dangerous is that it increases
the nerve cell membrane’s permeability to Na+ ions.
It is a lipid soluble compound and disrupts the integrity of the membrane.
• This causes spontaneous action potentials to occur all of the time.
o This seriously disrupts nerve cell transmission of information.
o This is how it kills insects! Nerves keep firing and insect is
stimulated to death.
• In humans, too much DDT affects the diaphragm and may result in
respiratory arrest.
o 1 billion kg produced in US alone. Takes decades to
decompose. Still produced overseas in poor countries.
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Local Anesthetics
Lidocaine and procaine (Novacaine) have the opposite effect of DDT.
(Also Marcaine with Epi, Carbocaine)
• They serve to decrease the permeability of the membrane to Na+ and
prevent action potentials.
o They act as a plug in voltage gated Na+ channels, so no
propagation of the action potential along the cell.
• This serves then to “numb” the localized area. See p. 400
• Tetrodotoxin (TTX) from puffer fish works in a similar manner.
• Ice can act to slow pain impulses by slowing down AP generation.
Histology (Cells) of the Nervous System
p 388-390
2 major categories of cells are found in the nervous system:
1. Nerve cells (neurons) – carry impulses and are electrically
excitable.
2. Glial cells (neuroglia)- do not carry impulses , not electrically
excitable.
We will discuss glial cells first.
Glial Cells (Neuroglia): table 12.1 p.392
• These cells do not carry electrical impulses as they are not
electrically excitable.
• About 9:1 ratio of glial to neurons, smaller, and make up half the
mass of the brain.
• You only need to know the Schwann cell by name and its function.
For the other glial cells, just know the function
There are several types of glial cells with a number of different functions.
Glial cells found in CNS:
See table 12.1 p 392-3
1. Astrocytes- most abundant, nutrient providers. Link between
neurons and blood vessels (part of blood-brain barrier).
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2. Oligodendroglia (oligodendrocytes)- produces myelin sheaths
around axons.
3. Microglia- derived from monocytes and act as phagocytes. Can
migrate to area of injury and infection.
4. Ependymal- ciliated semipermeable cells lining ventricles and
central canal. Makes CSF and helps it circulate.
Glial Cells found in PNS:
1. Satellite cells- surrounds and supports cell bodies of neurons in
ganglia.
2. Neurolemmocytes (Schwann cells)- produce myelin around
axons. Similar to oligodendrocytes in CNS in function.
Some of the many functions of glial cells are as follows:
1. Supportive of neurons - a "nerve glue". Like C.T.
2. Important in neuron nutrition.
3. Synthesize myelin.
4. Phagocytic.
Most brain tumors (gliomas) arise from the actively dividing glial cells
(neurons do not divide). Tumors arising from neurons can occur in young
children (<4yr) when neurons are still increasing in number.
Now, let’s discuss neurons.
Nerve Cells (Neurons): The nerve cells serve to carry electrical
impulses.
• They are electrically excitable.
• Other characteristics: extreme longevity, amitotic, high metabolic rate.
Fig. 12.3 p.389.
There are several structural neuron cell types (fig. 12.4 p.391) but we will
discuss a generalized type.
A typical neuron possesses the following characteristic features:
Fig 12.3 p 389
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2. nerve cell body (graded potentials (stimulus) received here)
myelin
node of Ranvier (neurofibral node)
nucleus
4. Axon terminal
1 . dendrite
synapse chemical activity here
3. axon (action potentials develop here)
direction of impulse
Diagram of a typical neuron with its component parts.
Generalized Nerve Cell (Neuron) Component Parts and Function
1. Dendrites
a. Serve to conduct information toward the nerve cell body.
b. This is the area of the nerve cell that receives input and exhibits
graded (chemically gated) membrane potential in response.
c. Are typically multiple and highly branched. (Receives stimuli
from other neurons).
d. Are generally shorter than axon.
e. Are irregular in size (diameter).
2. Cell body (soma)- contains the nucleus of the cell and typical
organelles.
a. Very active metabolically. Organized into ganglia in PNS and
nuclei (gray matter) in CNS. This is where graded potential are
developed.
3. Axon
a. This is the conducting portion of the neuron.
i. Serves to conduct the impulse away from the nerve cell
body, towards other neurons, muscle fiber, or a gland.
b. Generally single but end divides into many branches (10,000 is
not uncommon) forming axon terminals. Influences other
neurons or effectors (muscle, glands)
c. Longer, may be 3 feet (1 meter) in length.
i. Example: from spine to toe.
d. Of uniform diameter.
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The Axon structure in more detail.
Myelinated Axons
Fig. 12.3 p. 389
Some neurons are myelinated. p 392
• Myelin is a segmented sheath of fatty tissue (white matter) that
serves to increase the speed of the nerve impulse and insulated
neurons from each other.
• The amount of myelin increases from birth to maturity, so infants do
not respond as quickly or as coordinated as older children.
• Each segment of myelin is produced by a single glial cell (Schwann
Cell) that is wrapped around the neuron (up to 100 times).
• The areas between the myelin are known as nodes of Ranvier.
• The speed of conduction is greatly influence by 2 factors:
1. Diameter of the neuron, and
2. The myelin sheath.
Saltatory Conduction
fig. 12.13b p.403
1. Myelin Sheath
• The myelin causes the impulse to jump quickly from one node of
Ranvier to the next instead of traveling along the nerve cell
membrane by depolarization and action potentials.
• The myelin covers up the membrane so no ion leakage can occur. No
voltage gates are present in the membrane at this point.
• Local current flows the 1 mm distance to the next node quickly.
• At the next node, the membrane undergoes depolarization and an AP
develops to rebuild the current so it can travel to the next node.
Voltage gates are in high density at the nodes. Nodes slow things
down but current needs to be built back up.
• This speeds up transmission considerably, about 50x for myelinated
vs. unmyelinated fibers of comparable size
In summary, the jumping or skipping of the impulse that occurs in
myelinated fibers is known as saltatory conduction and carries information
much faster than in nonmyelinated neurons (gray matter).
2. Diameter
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• The greater the diameter of the myelinated neuron, the faster will be
its velocity of conduction - up to 120 meters per second
(360miles/hour) (e.g. the sciatic nerve)! Versus 0.7 m/sec for an
unmyelinated fiber that may service the digestive tract.
• Larger diameter means less resistance to current just as in copper
wire.
• Examples:
o Senses, action muscle: Type A, 5-20 um dia. 12-130m/s (27280 mph)
o Visceral sensory, motor: Type B, 2-3 um dia, up to 15 m/sec
o Sensory heat, cold,slow visceral motor: Type C, ½ - 1 ½ um dia
½ - 2 m/sec.
Multiple Sclerosis
Results from a disease of the myelin sheath in CNS and spinal cord. See
box, p 413
There is a progressive demyelination process (you lose the myelinated
sheath).
• MS is an autoimmune disease, a disease in which a person’s own
immune system produces antibodies that act against his or her own
healthy body tissues.
• It may be triggered by a viral infection. It affects over 2.6 million
people worldwide.
• Oligodendrocytes in CNS attacked by cytotoxic immune cells.
• The loss of myelin causes a decrease in the velocity of conduction of
the nerve impulse that can greatly effect coordination.
• Dx: 20-40 years old.
• There is a permanent scarring of the nerve tissue (plaques and scars
form) as the myelin sheaths are attacked.
• Beta interferon may help slow the disease. Steroids manage acute
attacks. Bone marrow transplants are experimental to remove
cytotoxic cells.
• Clinically, multiple sclerosis symptomology includes:
1. Numbness (when sensory neurons are affected.
2. Vision loss, double vision.
3. Uncoordinated movements.
• Attacks are followed by periods of remission.
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Temperature also affects the conduction of nerve impulses.
• A cold pack will help relieve some pain as pain nerves are partially
blocked by the cold.
Now back to the nerve cell parts and function discussion.
4.
•
•
•
•
•
Axon terminal (terminal bouton).
An axon terminal is the bulb shaped neuron ending.
This is the secretory or output component of the neuron.
It contains synaptic vesicles that contain neurotransmitter (chemical
messenger) that carries the nervous system message chemically
from one neuron to the next.
Message can be excitatory with ACh in NMJ or inhibitory ACh in
parasympathetic synapse with heart via vagus nerve (heart slows
down)
The neurotransmitter crosses a gap between the neurons known as a
synapse or from the neuron to a muscle cell across a gap known as
the myoneural junction (neuromuscular junction).
table 12.3 p 408 = Summary of neuronal structure and function.
Assignment Questions
Chapter 12
Describe the factors that give rise to resting potential.
Outline the steps in the generation and conduction of a nerve impulse.
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Types of Neurons
There are many different types of neurons in the body, some of which we
will discuss later.
For now we will limit our discussion to 3 types of neurons:
1. Afferent (sensory) neurons serve to bring the impulse or information
toward the brain.
2. Efferent (motor) neurons carry information out and away from the brain.
3. Interneurons (association or connector or internuncial) connect sensory
to motor neurons.
~90% of the neurons of the body are interneurons.
Now we will discuss and review some terms associated with neurons.
Physiological Properties of Neurons (Reviewed)
Threshold
•
Minimum strength (voltage) of a stimulus required to depolarize a
neuron (create an AP). Fig 12.11
• This is usually about –55 mV (membrane depolarizes about 15-20
mV from –70mV).
• This point is reached by the flow of Na+ across the membrane in
sufficient numbers per time.
Graded Potential
• These are the small potential changes in a local area of membrane
located where dendrites and cell bodies form a junction that is caused
by a stimulus, for example the binding of neurotransmitter.
• These can make the membrane more (hyperpolarized or inhibitory
postsynaptic potential IPSP) or less polarized (depolarized or
excitatory postsynaptic potential EPSP) fig. 12.10 p.398.
• When enough occur together at the axon hillock, they may trigger an
AP that travels down the axon to the axon terminal. See summation.
• They are not triggered by voltage-gated channels as AP but by
chemical, pressure, or light mechanisms.
Summation
Fig 12.15 p 407 discussion 406
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Two ways:
1. Temporal summation: Many subthreshold stimuli may act together in
an additive way to cause depolarization. This can occur by increases
the rate of stimulus (temporal summation) of a single presynaptic
neuron or
2. By several presynaptic (spatial summation) neurons firing to the
same postsynaptic neuron. These can be caused by combinations of
EPSPs and IPSPs with the outcome of an AP determined by the
presence of more EPSPs.
All or None Response
p 399
The response of a neuron to a stimulus is either maximal or not at all.
In other words, an action potential (AP) happens completely or not at all.
If enough Na+ does no enter the cell to trigger the voltage gates, no AP will
occur.
Refractory Period p 400 fig 12.11 p. 399 see boxes on right side of fig.
• The refractory period is a “resting period” for the neuron following
depolarization when a neuron cannot generate an other action
potential.
• Following depolarization, there is a period of time called an absolute
refractory period during which a second stimulus, no matter how
strong, will not elicit a response on the part of the neuron.
• The Na+ and K+gates are open or inactive, so repolarization is not
completed.
• In large diameter axons this period is 0.4ms, 4ms in smaller axons.
• In normal body conditions, maximum frequency of nerve impulses in
different axons is usually ranges from 10-1000/sec.
Adaptation (Accommodation) p. 502
• A continuous stimulus over and over eventually causes a rise in
threshold of the neuron; therefore it takes a greater stimulus to elicit a
response.
• The receptor neuron decreases its firing rate over time with the same
stimulus.
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• Receptors for touch adapt quickly (so you are not aware of your
clothes). Temperature receptors adapt between 20-40C but outside
this range do not adapt as the risk of tissue injury is substantial.
• Joint and muscle receptors adapt more slowly.
• Pain receptors do not generally adapt due to the survival value of
pain.
• In laymen’s terms there is a “deadening of the nerve”.
• Synonyms for accommodation would be habituation and tolerance.
• Other Examples
o For example, constant repeated exposure to a specific drug,
alcohol, or even noise may cause, in time, a reduced effect of
that stimulus.
o In other words, to achieve the same “high”, you may need more
of a specific drug.
The Nervous System Message
The nervous system message is electrochemical in nature.
1. The nerve impulse passes through the neuron as an electrical
message, and
2. Across the synapse as a chemical message.
• The chemical that carries the message across the synapse =
neurotransmitter.
• The nervous system message travels along distinct pathways =
nerves.
o (Unlike endocrine system where message travels via blood).
• A nerve is a bundle of neurons (actually bundle of axons or dendrites)
bound together by C.T. like the wire strands in an electrical cable.
The Synapse
Fig. 12.14 p.405
Although there are electrical synapses between cells in the cardiac muscle,
and some smooth muscle and CNS, we will only discuss the chemical
synapse found in most nerve to nerve (muscle) contact.
The Chemical Synapse
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• The synapse is an area of functional but not anatomical (structural)
continuity between one neuron and another.
o Therefore there is no structural connection.
• The synaptic cleft forms a chemical bridge 20-50 nm wide.
• The neurotransmitter serves to functionally connect the presynaptic
neuron to the postsynaptic neuron as it diffuses across the synapse.
• An AP triggers the opening of voltage Ca++ gates in the axon terminal
that triggers the exocytosis of neurotransmitter vesicles.
Physiological Properties of the Synapse
1. One way conduction
• Because only one end of the neuron contains synaptic vesicles with
neurotransmitter, the chemical message can only travel from the
axon terminal of the presynaptic neuron to the dendrites of
postsynaptic neuron.
See text p. 406 for next 2 terms. Also fig 12.10
2. Pre synaptic Facilitation or excitatory postsynaptic potential (EPSP)
• When an excitatory presynaptic neuron synapses with a postsynaptic
neuron that causes depolarization.
o The release of excitatory neurotransmitter to the postsynaptic
neuron excites the membrane and cause the membrane
potential to move towards 0mV (more positive) so it moves the
potential closer to triggering an action potential.
o This usually caused by a Na+ channel opening in the
membrane.
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3. Presynaptic Inhibition or inhibitory postsynaptic potential (IPSP)
• When an inhibitory presynaptic neuron synapses with a postsynaptic
neuron that causes hyperpolarization.
• Inhibition is the opposite of facilitation.
o The neurons is releasing an inhibitory neurotransmitter causing
further hyperpolarization of the membrane.
o This usually caused by opening a K+ or Cl- channel.
o The subtracts from any graded potential produced by a
excitatory synapse. It competes against an excitatory neuron to
create an action potential
o So, a greater excitatory stimulus is necessary for the message
(AP) to continue.
• Presynaptic facilitation and inhibition effects can last for minutes to
hours.
• They are of interest in terms of learning and memory.
Fig. 12.15 p.407
4. Summation
• Summation occurs when:
o Many presynaptic neurons converge on a single postsynaptic
neuron (spatial summation) or
o A single presynaptic neuron repeatedly fires in rapid succession
(temporal summation).
• You may have many subthreshold stimuli that work in an additive way
to produce enough neurotransmitter to meet the threshold of the
postsynaptic neuron.
o Example: The typical CNS neuron receives input from 100010,000 synapses.
5. Synaptic delay p 405
• The speed of the nervous system message slows at the synapse
because the electrical AP is converted to a chemical signal
(neurotransmitter) and then back to an AP.
• This is about a 0.5 ms delay.
• The velocity of the electrical message may be as high as 120 meters
per second along the neuron but chemical message slows to 0.5-1.0
ms at the synapse.
• Therefore the fewer the number of synapses to get the message from
one place to another, the faster it will travel.
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Other synapse notes
• Many drugs have great effect on the synapse; we have discussed
some of these.
o Aspirin causes sensory (pain) inhibition by raising the threshold
of conduction of impulses near the hypothalamus (pain center).
• pH
o Increased pH (basic condition, alkalosis) serves to increase the
ease of transmission, while lowering the pH (acidic condition,
acidosis) serves to depress transmission.
• O2 Hypoxia (low oxygen levels) can lead to cessation of synaptic
activity.
Types of Neurotransmitters
These are discussed in text p.407-410
• Neurotransmitters are present throughout the PNS and CNS.
• They may be inhibitory, excitatory, or both, depending on the
receptor!
• Some act on the membrane directly to open ion channels
while other activate secondary messenger systems in the
membrane that influence reactions inside the cell.
• About 100 are known.
Examples of neurotransmitters from the body follows:
1. Acetylcholine (ACh)
• Very common throughout the body as already discussed and is
continually broken down by acetylcholine esterase (AChE).
• Excitatory in neuromuscular junctions, but in inhibitory at
parasympathetic heart synapses.
Biogenic amines are certain amino acids that are modified and
decarboxylated. Depending on the receptor for these, they can be
excitatory or inhibitory.
Examples:
2. Norepinephrine (NE)
Derived from tyrosine.
• Found in CNS for roles in arousal from sleep, dreaming, mood.
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• Found in the PNS (postsynaptic neurons of the sympathetic division
of the nervous system). Also a hormone secreted from the adrenal
medulla to fortify a sympathetic response via the vascular system.
• Can be excitatory or inhibitory depending on receptor.
• The chemical structure of amphetamines is similar enough to mimic
norepinephrine.
o Therefore when a person takes amphetamines they exhibit a
sympathetic nervous system response that includes increased
heart and respiratory rate, dilated pupils, etc.
• Unlike acetylcholine that is continually broken down by acetylcholine
esterase, norepinephrine is removed from the receptor sites and
transported back across the synapse and back into the synaptic
vesicles to be used again and again.
o Cocaine is a drug that blocks the transport of norepinephrine
(and dopamine) back across the synapse.
o Therefore it makes sense that a person under the influence of
cocaine will exhibit a sympathetic nervous system response.
3. Serotonin (5-hydroxytryptamine (5-HT)) made from tryptophan
(amino acid)
• Found in the CNS involved in mood control, appetite, sleep induction,
temperature regulation.
• Serotonin is a neurotransmitter involved with behavior and has been
implicated in many psychotic disorders including depression and
others with hallucinatory symptoms.
• People with depression exhibit serotonin deficiency and
schizophrenia exhibit high levels (or dopamine too).
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o Prozac (fluoxetine), a commonly used antidepressant, is known
to inhibit serotonin reuptake and more is available in the
synaptic cleft.
• Mescaline, a drug found in peyote cactus, and LSD are known to
block serotonin receptor sites therefore bringing about hallucinations.
5. Amino acids
Several amino acids are neurotransmitters in the CNS.
Can be excitatory (glutamate) or an inhibitory neurotransmitter in the CNS.
Example of inhibitory:
GABA (Gamma Amino Butyric Acid)
• Found only in brain. Most common inhibitory neurotransmitter, in as
many as 1/3 of all brain synapses.
• It has a tendency to increase the cell membranes permeability via
chemically gated Cl- channels (as opposed to Na+ ions).
• This makes the cell membrane even more polarized and therefore
less excitable (inhibition). Antianxiety drugs diazepam (Valium)
enhances these effects.
• It is augmented by alcohol (slowed reflex coordination) and Valium.
Endorphins: concentrated in pituitary, thalamus, hypothalamus. Natural
opioid peptide. Relieves pain by inhibiting release of P substance from
sensory nerves.
Tetanus toxin (produced by bacteria introduced into a wound) prevents the
release of inhibitory neurotransmitters in neurons allowing all muscles to
contract simultaneously leading to a condition we call tetanus (lockjaw).
See table 12.3 p.408 for review of neuron structure and function
Components of a Spinal Reflex Arc
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fig. 13.5 p.427
• A reflex is a very fast involuntary response that serves to prevent
bodily harm.
• Said another way, they are programmed, stereotyped, predictable
motor responses to specific sensory stimuli.
• These make up the behavior of simpler animals.
• There are few synapses and the message only has to travel to the
spinal cord (not the brain) for you to respond, therefore your response
is very quick.
o Many brain reflexes exist (eye movement, sneeze, etc., but we
will not discuss)
Example: Jerking your hand back from a hot flame.
A withdrawal reflex or a limb flexor reflex. Fig 13.8 p 431
1. Receptor - a sense organ detects a stimulus (heat receptor in this
case).
2. Afferent neuron - serves to carry the information to the spinal cord
(integrating center).
3. Interneuron - is found within the spinal cord and connects the afferent
(sensory) neuron to the efferent (motor) neuron.
a. This is the integrative function leading to the stimulation of the
flexors.
4. Efferent neuron - carries the motor information from the spinal cord to
the effector organ in the periphery.
5. Effector organ - a motor effector (skeletal muscle in this case) that
contracts and causes you to jerk your hand back.
Questions
Chapter 12
Describe presynaptic facilitation and inhibition.
Describe spatial and temporal summation.
Chapter 13
What is a reflex arc? List and define the components of a reflex arc and describe how
the spinal cord serves as an integrating center for reflexes.
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The Central Nervous System
The Brain
Development of the Brain
Text p 490-491 Fig. 14.25 p.490
• The nervous tissue begins as a thickening of the embryonic ectoderm
that forms a neural plate.
o The plate rounds to form a groove.
o As the edges of the groove meet they form the first early
structure, a tube.
o So, brain begins as a simple tube, a neural tube.
• The tube or chamber (ventricle) is filled with cerebrospinal fluid.
o The cerebrospinal fluid serves to cushion the brain and spinal
cord.
Nervous tissue
Chamber (ventricle) filled with fluid called cerebral spinal fluid.
CSF serves to cushion brain.
View a 3-4 week embryo brain
Fig. 14.26a left, p.491
See an early CNS with forebrain, midbrain, and hindbrain, with the spinal cord
descending.
• With time we see further development of the brain and can see the
major brain divisions (primary vesicles) begin to appear. Soon, the:
o Forebrain (proencephalon),
o Midbrain (mesencephalon), and
o Hindbrain (rhombencephalon) become apparent.
View a 5- week old embryo brain
Fig. 14.26b p.491. See where the subdivisions of the brain develop.
As development proceeds, these 3 fluid filled vesicles undergo further
bending and constriction forming 5 secondary vesicles as follows:
1. Forebrain (Prosencephalon) becomes the telencephalon and
diencephalon.
a. The telencephalon will become the cerebrum (2 hemispheres, basal
ganglia (nuclei), 2 lateral ventricles).
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b. The diencephalon will become the thalamus (3rd ventricle), and
hypothalamus.
2. Midbrain (mesencephalon) becomes the mesencephalon (with cerebral
aqueduct).
3. Hindbrain (rhombencephalon) becomes the metencephalon and
myelencephalon.
a. The metencephalon becomes the pons, and cerebellum.
b. The myelencephalon becomes the medulla oblongata.
Use fig. 14.1 p. 453 See a developed brain
With greater development, we begin to see extensive convolutions of the
cerebrum above, and the cerebellum below.
This folding allows for more neurons to fit is a limited space (the skull).
Formation of the Spinal Cord
• The neural tube inferior to the myelencephalon becomes the spinal
cord.
• 2 neural tube defects, spinal bifida (lack of closure of the vertebrae)
and anencephaly (absence of skull and cerebral hemispheres) are
associated with low levels the B vitamin folic acid.
o So, folic acid supplements are important for a healthy
pregnancy.
Component Structures of the Brain
figure 14.1 p. 453 table 14.1
Telencephalon
Cerebrum
p. 467
Function
The cerebrum perceives information, directs motor responses, and, is the
center of intellect, memory, language, and consciousness.
Structure
The cerebrum is subdivided by convolutions.
Fig. 14.11 p.468
In terms of the convolutions:
• Grooves or depressions are called a sulcus (sulci) or fissure.
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• Rounded or elevated portions of the convolutions are called a gyrus
(gyri) .
• It is important to note that the convolutions are not a random pattern.
• The longitudinal fissure divides the cerebrum into right and left halves
called cerebral hemispheres.
o Within each of the hemispheres, the fissures divide the
cerebrum further into lobes.
• The lobes of the cerebrum are located on its outer surface known as
the cerebral cortex.
• The cerebral cortex is the gray matter of the cerebrum. An outer rim
(2-4 mm) of gray matter.
• It consists of approximately 12 to 15 billion nonmyelinated neuron cell
bodies and associated glial cells.
• The gray matter is the computer of the CNS and the white matter the
wires that interconnect the computing areas.
• The cerebrum accounts for 80% of the brain weight and the human
cerebrum is the most developed of all species.
Lobes of the Cerebral Cortex
Fig. 14.11 p.468
The lobes of the cerebral cortex are named for the bones of the
cranium that overlay them.
Note locations on fig. 14.11
Functions:
Fig. 14.15 p. 474
1. Frontal Lobe
• The frontal lobe is a primary motor area, also known as the
somatomotor area. Fig 15.5 p. 508.
o It is responsible for voluntary movement. See the primary motor
(#4), area located in the precentral gyrus. Note: ALS
(amyotrophic lateral sclerosis, Lou Gehrig’s disease) attacks
this area, as well as the lateral white columns, and lower motor
neuron cell body’s.
• It is also responsible for speech in part (Broca’s area (#44)).
• It is separated from the parietal lobe by the central sulcus.
• It is separated from the temporal lobe by the lateral cerebral sulcus.
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2. Parietal Lobe
• The parietal lobe is a general sensory area.
o Examples: touch, pressure, heat, cold, pain.
• It receives and processes sensory input. Fig 15.5a
• Therefore it is completely afferent in its function.
• It is separated from the occipital lobe by the parieto-occipital sulcus.
3. Occipital Lobe
• The occipital lobe is primarily responsible for processing visual input
or vision.
• It is sometimes called the visual cortex.
4. Temporal Lobe
• The temporal lobe is the auditory area where sound sensation is
received and associated with speech, music, or noise.
• It is of primary importance for hearing and some speech.
• It is sometimes called the auditory cortex.
As stated earlier, the fissures that can be seen on the lobes of the cerebral
cortex are not a random pattern.
• The fissures serve to separate areas of the brain with different
functions.
• About 100 different functions have been isolated for different
convolutions of the brain.
How was this determined?
• This was originally done by inserting electrodes into different parts of
the brain and monitoring the activity of the brain.
• Also, people with specific brain damage have provided invaluable
information.
• New equipment, is less invasive.
o MRI with computers can now monitor the slight temperature
changes that take place in the brain as blood flows into areas
that become active during different activities.
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White Matter of the Cerebrum
P 469
The white matter of the cerebrum is located beneath the cerebral
cortex.
It consists largely of myelinated fibers bundled into large tracts.
• They functions as wires that allow interaction between parts of the
cerebral cortex or other areas of the brain.
• This integration is essential for even the simplest of tasks.
• Example: picking a flower and enjoying (vision, fragrance, movement,
beauty, etc)
They are organized into tracts and are classified according to
which direction they run into of 3 types of fibers:
Fig. 14.12 p.408
1. Commissural Fibers
Structure:
Commissural fibers serve to connect the corresponding areas of the 2
cerebral hemispheres (right and left brains).
Example:
Fig 14.9 p 469
• The largest structure they comprise is called the corpus callosum.
Function:
• Coordinates actions on both sides of the body.
2. Projection Fibers
Structure:
• These fibers form ascending and descending (vertical) tracts that
connect the cerebrum to the lower brain, spinal cord.
• Example: See the Internal Capsule just lateral to the thalamus, which
then continues as the corona radiata to the cortex. fig. 14.13b p.470.
• Also see projection tracks. Fig 14.2 p469
Function:
• Projection fibers serve to connect the cerebral cortex to the lower
brain and spinal cord. They tie the cerebrum to the rest of the
nervous system and to the receptors and effectors of the body.
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3. Association Fibers
Structure:
• These tracts connect gyri within a hemisphere.
• Short fibers connect adjacent gyri and long fibers connect different
cortical lobes.
• Example: Association fibers. Fig 14.12
Function:
• Transmit impulses between gyri in the same hemisphere.
• One role is to link perceptual and memory centers, so you can
associate a smell with a thing.
Basal Ganglia (nuclei)
P 469-71 Fig. 14.13 p.470
The deep area of white matter of the cerebrum also contains
several groups of nuclei called the basal ganglia (3 masses of
gray matter in each hemisphere).
Function:
• Regulates motor functions executed by the cortex, regulates muscle
tone, and coordinates rhythmic movements (e.g. arm swinging while
walking).
• Important in starting and stopping movements and the intensity of
movement.
• Other functions too related to cognition and emotions.
Parkinson’s disease p 515, 521
• The basal ganglia cells that degenerate have been implicated in
Parkinson’s disease also known as shaky palsy.
• The loss of dopamine releasing cells in the basal nuclei causes an
increase in tone.
• Parkinson’s disease appears in people in the age group of 50 to 65
and causes tremors of the limbs, slow movements, and postural
changes (stiffness of face, arms, and legs).
• It may be caused by environmental toxins or pesticides.
Huntington’s disease p 515
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• An inherited (autosomal dominant) condition, causes overstimulation
of the motor drive.
• Loss of neurons in the basal ganglia that release GABA or ACh.
• Key sign is chorea: Limbs jerk unstoppably in a dance like manner.
• Onset at 30-40, then death within 10-20 years.
Asymmetry of the Brain or Brain Lateralization
p. 475-476 table 14.2 p. 477
• The brain can be thought of as 2 hemispheres connected by a bundle
of nerve fibers called the corpus callosum (commissural fibers).
• Sensations from one side the body are most commonly perceived in
the cerebral hemisphere on the opposite side of the body.
• Example: Vision of the left eye is controlled by the right hemisphere,
and vice versa.
The 2 cerebral hemispheres are asymmetrical in some structure and
function.
• If the left temporal lobe of the brain is damaged, you will commonly
observe language difficulties.
o If the right temporal lobe is damaged, there are no such
difficulties.
• In dyslexia (difficulty in reading), the left temporal lobe is typically
smaller than a right.
• The 2 hemispheres of the cerebrum have the following
responsibilities:
Left hemisphere
Speech
Language
Analytical problem solving
Control of right side
Right hemisphere
Visual -- spatial relationships
Dreaming/imagination
Musical and artistic ability
Control of left side
• A right handed person will have a larger left temporal lobe, left
occipital lobe, and right frontal lobe.
o 90% of people are left hemisphere dominant.
• A left handed person usually has right hemisphere dominant of no
asymmetry (may be ambidextrous).
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Diencephalon — thalamus and hypothalamus
Thalamus
P 464-465 fig. 14.9. p.464.
• It is composed of paired oval masses of gray matter organized into
nuclei.
• The thalamus is a relay center for sensory information received from
the spinal cord, cerebellum, and brain stem going to the cerebrum.
• It can crudely sense pain, temperature, and pressure.
• It plays an important role in cognition: awareness and acquisition of
knowledge.
• Epithalamus:
o Superior and posterior to the upper portion of the thalamus is
the epithalamus that contains the pineal gland.
o The pineal gland secretes melatonin, a hormone, and controls
sleepiness and biological rhythms (biological clock).
Hypothalamus
P 466-467 fig. 14.10 p.466.
• The hypothalamus is a collection of nuclei and associated fibers that
lie beneath the thalamus.
• The hypothalamus is extremely important.
• It is an integrating center for important homeostatic functions and
serves as an important link between the autonomic nervous system
and the endocrine system.
• It secretes several hormones that influence the pituitary gland.
• Many axons extend to sympathetic and parasympathetic nuclei in the
brain stem and spinal cord.
It controls many vegetative (or visceral) functions (regulation of the internal
environment).
• That is, functions not under voluntary control.
• In other words, these things happen without thinking of them (you are
vegetating!)
• The hypothalamus is of primary importance in the maintenance of
homeostasis.
Functions of Hypothalamus:
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1. Control of the pituitary gland, the master gland of the endocrine
system.
2. Body temperature regulation via ANS.
3. Control of appetite (food intake).
4. Water balance (urine output via ADH secretion) and intake (thirst).
5. Controls and integrates activities of the ANS. Main regulator of
visceral activity. Examples: Gastric secretion, heart rate, GI food
movement
The hypothalamus is also involved in emotion as a part of the limbic
system. fig 14.14 p 471
• The limbic system or the ‘emotional brain’ is important in the
expression of fear, rage, aggression, pain, pleasure, and instinctual
sexual behavior. It is located encircling the brain stem and corpus
callosum.
• The limbic system has special neurotransmitters called endorphins
that are natural opiates that lessen pain and stress.
• Its evolutionary age (600 million years) is much older than the cortex
(60 million years).
Now, on to the brain stem (midbrain, pons, and medulla)
Most of the cranial nerves arise from the brain stem.
Mesencephalon or midbrain
P 460-462
Fig. 14.7 p.461
The midbrain serves a relay center between the forebrain and hindbrain.
Contains the cerebral aqueduct which connects the 3rd and 4th ventricles.
Several reflexes are controlled here.
Examples:
Eye, head, neck movements in response to visual and other stimuli.
Metencephalon — Pons and Cerebellum
Pons
P 459-460 fig. 14.8c p.463.
• The pons lies directly superior to the medulla and anterior to the
cerebellum.
• It has both nuclei and white matter.
• It acts as a bridge connecting the spinal cord with the upper brain.
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• It helps control breathing with the hypothalamus.
• The pons also relays motor information from the cerebrum to the
cerebellum.
Cerebellum
P 462-463 fig. 14.8 p.463
• The second largest portion of the brain and lies in the inferior and
posterior area of the cranial cavity.
• The cerebellum is the center for motor coordination of complex body
movements. It evaluates how well movements initiated by the cortex
are actually being carried out.
o It compares the motor output from the cortex with the sensory
input from proprioceptors in muscles, tendons, and joints, and
receptors for equilibrium and vision.
o The cerebellum sends feedback to the motor area to correct
activity of skeletal muscle.
• It is also important in maintaining equilibrium (balance) and in the
coordination of antagonistic muscles (posture).
• So, it makes possible all skilled motor activity: dancing, catching a
ball, etc.
Myelencephalon — Medulla oblongata
p. 458 Fig 14.6 p 460
• The medulla oblongata is continuous with the spinal cord and begins
at the foramen magnum and ends at the pons (about 3cm).
Sometimes called the brain stem.
o However, the brain stem includes the midbrain, the pons, and
the medulla oblongata.
• The medulla oblongata serves to regulate some vital and nonvital
body functions.
Vital functions
Respiration center (breathing rhythm)
Heart rate and force (cardiac center)
Blood vessel diameter (vasomotor center)
Nonvital Functions
Sneezing
Coughing
Vomiting
Swallowing
Hiccuping
Blows to the back of the head or upper neck can be fatal due to the vital
activities of the medulla.
Physiology 7
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• The medulla oblongata is where the crossing of fiber tracts
(decussation) takes place and is responsible for the right side of the
brain controlling what takes place on the left side of the body and vice
versa. About 90% of the fibers cross here.
Reticular formation
P 462
• The reticular formation is found within the brain stem and regulates
consciousness, that is, whether you are awake, sleeping, or
dreaming. Fig 15.10 p518
• It is a located throughout the brain stem where white and gray matter
are interspersed in a net like configuration.
• It alerts the cerebral cortex to incoming sensory signals.
o This is called the reticular activating center (RAS). P. 517
o It is responsible for maintaining consciousness and awakening
from sleep by arousing the cortex.
o The RAS responds to incoming impulses: ears (alarm clock),
eyes (light of morning), or painful stimuli that arouse the cortex.
Note: no olfactory input so may be over come by smoke in
sleep. Therefore, have a smoke detector in sleeping areas.
• The main descending function is maintenance of muscle tone.
Consciousness, emotions, learning and memory.
We will leave these topics for your psychology class! Found in chapter 15 p.
519-520 if interested.
Blood supply to the brain.
p. 492
A cerebrovascular accident (CVA) occurs by:
1. Ischemic event, or
2. Hemorrhage due to vessel rupture.
Will appear as an abrupt onset of neurological deficits such as paralysis or
loss of sensation.
We will discuss this in more detail with the cardiovascular system
discussion.
Exam II
Multiple choice
Matching
3 essay 3x5=
Physiology 7
50 pts
10 pts
15 pts
75 total points
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