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Physiology of Nerve and Muscle
I. Nerve
Nerve cell is called neuron. There are 100 billion neurons (give or take 100
million) differ based on their structure, chemistry and function. Neurons confer
the unique functions of the nervous system. Glia are the supporting elements
which are 10 times as many as neurons.
Neurons contain the same basic structures as most other cells; Cell body
(soma or perikaryon) and neurites (axons and dendrites). Cell body usually
gives rise to a single axon which conducts nerve impulse from one neuron to
the next. It is up to 1 meter in length. The speed of the nerve impulse is a
function of the diameter of the axon. Dendrites are small (rarely more than
2mm) and organized symmetrically (antennae). The term dendritic tree is a
collective term for all neurites of a given neuron. Neural signals are either
efferent (away from the cell body) or afferent (towards the cell body).
Fig: 1
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1. Types of glia in CNS:
a. Astrocytes: Most abundant, most versatile. Their numerous processes cling
to neurons and their synaptic endings, and cover nearby capillaries. So they
support and brace the neurons and anchor them to the nutrient supply lines.
They have a role in making exchange between capillaries and neurons, in
helping determine of capillary permeability, guiding migration of young
neurons and in synapse formation. Regulate extracellular space, mopping up
leaked potassium ions, restricting and recycling neurotransmitters. They are
connected to each other by gap junctions and signal each other both by taking
in calcium (calcium pulse or calcium sparks) and by releasing extracellular
messengers. Recently it is found that astrocytes participate in information
processing in the brain
Fig: 2
b. Microglia: Migrate toward injured or troubled neurons and transform into
special type of macrophages. So they are the scavenger cells that get rid of
microorganisms or neural debris.
c. Ependymal cells: Line the central cavities of brain and spinal cord.
d. Oligodendrocytes: Myelinating glia in central neurons that form myelin
sheath (what holds a sword) which wrap around the axons to function in
insulation.
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Fig. 3:
2. Types of glia in PNS:
a. Schwann Cells: Produce myelin sheath and neurilemma in peripheral
neurons. In addition to insulation, they aid in regeneration of damaged
peripheral nerve fibers.
b. Satellite cells: Surround cell bodies in PNS and have many of the same
functions as astrocytes in CNS.
Fig. 4
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Classification of nerves
1. Physioanatomic classification: Neurons are classified into afferent
(sensory) and efferent (motor). Each is subdivided into somatic and visceral
neurons. The latter subdivisions are further subdivided into general and
special neurons.
2. Another classification is according to conduction velocity and caliber of
nerve fiber. From larger to lower caliber they are:
Nerve type Aα has the largest diameter and fastest conduction velocity e.g.
somatic motor and proprioceptive nerve fibers.
Nerve type Aβ e.g. sensory fibers of fine touch and fine pressure.
Nerve type Aγ e.g. motor fibers to muscle spindle.
Nerve type Aδ e.g. sensory fibers of acute pain, crude touch and cold.
Nerve type B e.g. preganglionic autonomic nerve fibers.
Nerve type C has the smallest diameter unmyelinated fibers e.g. sensory
fibers of chronic pain, heat, gross pressure and postganglionic sympathetic
fibers.
Resting membrane potential
All living cells (whether animal or plant cells) exhibit potential difference
across their plasma membranes when microelectrodes are inserted into these
cells where the membrane interior is negative in relation to the membrane
exterior. This is called resting membrane potential (RMP) and it is due to
uneven distribution of ions inside and outside the membrane.
Ion
Extracellular
Intracellular
Na+
K+
Cl–
Phosphates
Proteins
142 mEq/L
4 mEq/L
103 mEq/L
4 mEq/L
30 mg/dL
10 mEq/L
140 mEq/L
4 mEq/L
75 mEq/L
200 mg/dL
Accordingly, RMP of nerve cell is –70 mV, RMP of skeletal muscle is –90
mV, RMP of cardiac muscle is –85 mV, and lastly RMP of smooth muscle is
variable but nearly about –50 mV.
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The following ionic fluxes are responsible for the electric phenomenon of
resting membrane potential:
1. Sodium-Potassium pump: This is called Na+-K+ ATPase pump which
extrudes three sodium ions outside the cell and intrudes two potassium
ions inside. This results in much positive ions outside plasma membrane.
2. Sodium channels are inactive at rest. They are voltage gated channels i.e.
they are activated by electric current. This means that sodium influx is
not possible unless membrane potential is changed from resting to action
potential.
3. Potassium channels allow continuous passive diffusion of K+ outside the cell
due to concentration gradient. This K+ efflux results in diffusion
potential and increased positive charges outside plasma membrane
which is the major factor responsible for resting membrane potential.
4. Chloride ions stand still inside the cell due to their higher concentration
outside the cell. This conserves negative charges inside plasma
membrane.
5. Anionic proteins and phosphates can not leave the cell due to their large size
making plasma membrane impermeable to their efflux. This adds to the
negativity of plasma membrane interior.
Fig. 5
PROTEINS¯
3Na
PHOSPHATES¯
CHLORIDE¯
+
Pump
2K+
K+
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Local responses and action potential
Nerve and muscle cells are excitable cells i.e. they have the ability to
reverse the negativity of their membrane potential in response to a sufficient
external stimulus. The external stimulus may be electrical, chemical, physical
or other types of stimuli. This change in membrane potential is called action
potential. The response in nerve cell is transmission of action potential (nerve
impulse) while the response in muscle cell is contraction.
Fig. 6: Curves of local responses and action potential in neuron
Overshoot of
depolarization
Repolarization
Depolarization
RMP
Threshold
↑↑L o c a l ↑↑ r e s p o n s e s ↑↑
Hyperpolarization
Weak external stimuli when applied to the neuron may cause local
responses which may increase or decrease with the charge and amplitude of
stimuli and the responses subside after removal of these stimuli. Local responses
may be cathodal (+ve) or anodal (-ve). Catelectrotonic stimuli cause less
negative membrane potential, while anelectrotonic stimuli cause more negative
membrane potential.
When a sufficient stimulus raises the membrane potential 15 mV above
RMP (i.e. from –70 mV to –55 mV); action potential phases will start and does
not stop until complete cycle occurs. This is called all-or-none rule. The
membrane potential at which action potential starts is called threshold
potential or firing potential. Subthreshold stimuli may not affect the
membrane potential or cause only local responses while supramaximal stimuli
induce the same effects as threshold stimuli and do not change the shape of
action potential curve.
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The phases of action potential curve in neurons are:
1-Depolarization phase: Sharp rise of curve toward zero membrane potential
which overshoots to reach about +35 mV. This phase is due to activation of all
fast Na+ channels with inrush of huge number of Na+ ions causing plasma
membrane to lose its negativity.
2-Repolarization phase: Rapid fall of the curve toward the previous negative
potential which occurs due to fast inactivation of Na+ channels and continuous
pumping of Na+ and passive diffusion of K+ outside the cell.
3-Hyperpolarization phase: Decline of the curve to a more negative potential
than RMP which is here about –72 mV and it is due to slow closure of K+
channels. After that, the membrane regains its RMP.
Any stimulus, however large, does not induce any new action potential at
time of previous depolarization until third repolarization is complete. This is
called absolute refractory period because Na+ channels cannot be reactivated
immediately after previous activation.
From the point of third repolarization to the end of repolarization phase a
stronger stimulus is needed to induce new, but weaker, action potential because
fewer Na+ channels can be activated. This is called relative refractory period.
1/3 repolarization
Relative
refractory
period
Absolute
refractory period
Depolarization
Fig. 7:
Full repolarization
Threshold
Calcium ions stabilize the membrane by increasing threshold potential
﴾toward more positive position﴿ so, lack of Ca++ results in lower threshold
potential which makes the membrane very excitable and continuously firing
﴾tetanus﴿.
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Propagation of action potential
Action potential is triggered in axon hillock due to presence of large number
of Na+ channels and transmitted along the axon. The huge number of positive
charges inside the firing segment of membrane will be equilibrated by the
adjacent segments resulting in electrotonic flow of current which is very fast
(like in the solid electricity wire).
Nerve fiber is not a solid wire, instead, it is leaky and surrounded by sea of
electrolytes. So, the impulse will gradually subside unless there are new AP
waves at the adjacent segments of the axon.
Every new wave will cost time (0.1 milliseconds for each AP) which will
extremely delay the transmission of impulse. Myelin sheath provides insulation
to prevent leakage of ions and, hence, increases conduction velocity.
Fig. 8: Electrotonic flow of current
Insulation is interrupted at regular intervals by nodes of Ranvier which act
as augmentation stations to strengthen the ongoing wave of depolarization by
triggering new AP waves because these nodes are rich in Na+ channels. This is
called saltatory conduction because it is jumping from node to node (See
figure 9).
It travels in only one direction from soma to axon terminal (orthodromic
conduction) and not in the opposite direction (antidromic conduction)
because when action potential leaves certain segment, it cannot return
immediately to the same segment that passes an absolute refractory period. So,
it proceeds forward to a new resting segment not backward to the recovering
refractory segment.
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Fig. 9: Saltatory conduction
Synaptic and junctional transmission
Synapse is the junction between two neurons. The first is called
presynaptic neuron and the other is called postsynaptic neuron. Between
them is the synaptic cleft.
Fig. 10:
Presynaptic N
Synaptic cleft
Postsynaptic N
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Synapses are either chemical or electrical. Electrical synapses are very rare
in adult mammalian nervous system. Gap junction is an example of this type
where current flows directly through a specialized protein molecule
(connexon). The distance between two sides of membrane is very small (5nM).
Chemical synapses are the predominant type of synapses where chemical
substances called neurotransmitters (NT) are synthesized and stored in
synaptic vesicles.
When AP arrives at the axon terminal, it opens voltage gated Ca2+ channels
(channels that are opened or closed electrically) and Ca2+ influx will increase
intracellular Ca2+ concentrations which attract the synaptic vesicles (full of NT
substance) to the presynaptic membrane and signals the NT to be released to
the synaptic cleft by exocytosis.
Vesicles fuse with the active zones of presynaptic membrane. NT diffuses
across the synaptic cleft to bind its specific receptor on the postsynaptic
membrane.
Several types of neurotransmitters are available and each may have several
types and subtypes of receptors. Postsynaptic action depends on the nature of
the receptor. After that, NT must be inactivated by degradation, reuptake,
diffusion, or bioconversion.
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Properties of synapses:
1- One-way conduction from pre- to post-synaptic neurons because post
synaptic membrane contains no synaptic vesicles.
2- Synapse is a site of neurotransduction (from electrical to chemical signal).
3- Intercellular chemical messages converted into intracellular signal.
Fig. 11:
(Ionotropic)
(Metabotropic)
4- Synaptic potentials are either excitatory (EPSP) or inhibitory (IPSP). EPSP
bring the membrane potential toward threshold (depolarize) i.e. cations in or
anions out while IPSP move membrane potential away from threshold
(hyperpolarize) i.e. anions in or cations out.
5- EPSP and IPSP are present simultaneously in synaptic cleft.
6- Synaptic potentials are not all-or-none potentials.
7- A period of time (about 0.5 ms) is required for the signal to travel from pre- to
post-synaptic neurons which is called synaptic delay.
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8- Events are summed over time and space (spatiotemporal summation).
Effects may be additive or subtractive. Arrival of impulses from numerous
synaptic knobs on the same neuron at the same time is called spatial summation
and arrival of multiple successive impulses at the same synaptic knob is called
temporal summation.
Temporal summation
Spatial summation
9- Several presynaptic neurons may converge on single postsynaptic neuron.
Convergence
10- Single presynaptic neuron may diverge by its axon and its collaterals into
several postsynaptic neurons.
Divergence
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11- Axon collaterals from postsynaptic neurons may reverberate to the
presynaptic neuron(s).
Reverberation
12- Occlusion means that the sum of activities of several neurons working
together is less than the sum of their activities when they work separately.
Works separately on 2 neurons
Works separately on 2 neurons
Works separately on 2 neurons
Total together work on 4 neurons
Total: separately work on 6 neurons
13- Several successive EPSP may facilitate the synaptic knob to depolarize while
several successive IPSP may inhibit the synaptic knob.
14- Continuous recurrent weak synaptic potentials may cause habituation of
postsynaptic neuron which will not respond for similar future stimulations while
recurrent strong stimulations accompanied by other weak stimulations may cause
sensitization of postsynaptic neuron.
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Classification of neurotransmitters
Two groups of synaptic transmitters
A. Small molecule, rapidly acting transmitters:
Class I: Acetylcholine
Class II: The amines (adrenaline "epinephrine", noradrenaline
"norepinephrine", dopamine, serotonine and histamine).
Class III: Amino acids (γ-aminobutyric acid "GABA", glycine, glutamate
and aspartate).
Class IV: Nitric oxide "NO".
B. Neuropeptide, slowly acting transmitters:
a- Hypothalamic-releasing hormones.
b- Pituitary peptides.
c- Peptides that act on gut and brain.
d- Peptides from other tissues.
Criteria for classification as a neurotransmitter
a. Molecule must be synthesized and stored in the presynaptic neuron
b. Molecule must be released by the presynaptic neuron upon stimulation
c. Application of the neurotransmitter directly to the target cell must be shown
to produce the same effects as the response produced by the release of the
neurotransmitter from the presynaptic neuron.
Many neurons release more than a single neurotransmitter. Neurons that use
particular neurotransmitters are accordingly named cholinergic (use acetylcholine), catecholinergic (catecholamines: epinephrine, norepinephrine,..),
serotonergic (serotonine), amino acidergic ( amino acids), and so on...
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Acetylcholine
ACh is the neurotransmitter for neuromuscular junction, preganglionic
neurons of the sympathetic and parasympathetic PNS, postganglionic neuron of
the parasympathetic PNS and basal forebrain and brain stem complexes.
ACh is synthesized from acetyl coenzyme A and choline. The reaction is
catalyzed by choline acetyl transferase enzyme (CAT).
CAT
Acetyl coenzyme A + choline
Acetylcholine
Acetylcholine is degraded in the synaptic cleft by acetylcholinesterase
enzyme (ACE).
ACE
Acetylcholine
choline + acetate
ACh receptors are nicotinic receptors (protein complex comprised of 5
subunits: subunits are either alpha or beta) and muscarinic receptors. Nicotinic
receptors are present in neuromuscular junction, sympathetic ganglia and
many parts of CNS. Muscarinic receptors are present in smooth muscles and
glands.
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II. Muscle
Fig: 12
I. Skeletal muscle: General functions of skeletal muscle are:
Movement
Maintenance of posture
Stabilization of joints
Temperature homeostasis
It is striated voluntary muscle surrounded by epimysium and composed of
fasciculi. Each fasciculus is surrounded by perimysium and composed of
muscle fibers (elongated muscle cells). Muscle fibers are separated from each
other by endomysium and each muscle fiber is surrounded by sarcolemma
(plasma membrane) and composed of sarcoplasm (cytoplasm of muscle cells),
myofibrils, multiple nuclei, mitochondria and sarcoplasmic reticulum in
addition to other cellular components. Myofibrils are composed of
myofilaments (thick and thin contractile elements of skeletal muscle which
give the muscle its striation).
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The functional unit of skeletal muscle is called sarcomere which is
composed of the following compartments:
1. A bands (dark anisotropic bands) composed of myosin thick filaments.
2. I bands (light isotropic bands) composed of parts of actin thin filaments not
overlapped by myosin.
3. H band (within A band) visible only in relaxed muscle.
4. M line (bisects H band).
5. Z disc (midline membrane in I band connecting myofibrils together).
Sarcomere is region of myofibril between two successive Z discs.
Fig: 13
H zone
I band
A band
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Thick filaments: Myosin is rod like tail that terminates in two globular
heads. The tail is comprised of heavy meromysin (two interwoven
polypeptide chains). The head is comprised of light meromysin.
Thin myofilaments: Is comprised of G (globular) actin arranged in double
stranded helix and two regulatory proteins which are:
1- Tropomyosin (spirals around actin and blocking myosin head binding
sites during relaxed state)
2- Troponin (polypeptide complex). Troponin is composed of three
subunits:
1.Troponin C (TnC) binds Ca2+
2.Troponin T (TnT) binds tropomyosin
3.Troponin I inhibitory protein (TnI) that binds actin
Troponin-tropomyosin complex attached to actin filament. Tropomyosin
positioned to block myosin binding sites on actin filament. ATP and inactive
ATPase bound to myosin head.
Sarcolemma continues as inward invaginations of various depths called T
tubules which are in close proximity to sarcoplasmic reticulum on either
side. This is called sarcotubular system which is of great importance in
transmission of the propagated action potential wave along sarcolemma deeply
via T tubules resulting in release of Ca2+ from sarcoplasmic reticulum stores to
be near the myofibrils.
Fig: 14
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Contraction of Skeletal Muscle
Sliding filament theory of Contraction (excitation contraction coupling)
1- Nerve impulse (afferent signal) from motor neuron arrives motor end
plate (neuromuscular junction) resulting in release of Ach into the synaptic
cleft to bind nicotinic receptor on post synaptic membrane which opens Na +
channels and generates action potential in sarcolemma.
2- AP propagates along sarcolemma and down T tubules resulting in release
of Ca2+ from sarcoplasmic reticulum to the myofibrils.
3- Myosin ATPase is activated and ATP splits resulting in high energy
myosin-ADP complex.
4- Ca2+ binds to troponin resulting in changes in molecular shape of
troponin.
5- Tropomyosin is removed from binding site of myosin on the actin
filament and myosin attaches to actin (actin-myosin cross bridge).
6- Potential energy stored in high-energy configuration is used to pivot
myosin head. Myosin head bends as it pulls on actin.
7- ADP and inorganic phosphate are released from myosin.
8- New ATP attached to myosin head and cross bridge simultaneously
detaches.
Following death, there is no ATP and muscle fibers cannot relax (rigor
mortis). If no new impulse, Ca2+ is pumped back into sarcoplasmic reticulum
(SR) and relaxation occurs. If Ca2+ present from additional impulse, cycle
repeats and myosin head “steps” to next binding site on actin.
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Motor unit
Motor unit is a single motor neuron + its collaterals and skeletal muscle
fibers they supply. Motor unit could be small in size (few collaterals arise from
motor nerve to supply few muscle fibers) or large in size (so numerous
collaterals and muscle fibers). Three types of muscle fibers are found:
Slow oxidative fibers (slow red)
Fast oxidative fibers (fast red) which is very rare in human.
Fast glycolytic fibers (fast white)
Skeletal muscle is a mixture of these three types of fibers, so there are red
muscles and white muscles.
Red muscles contain higher percentage of red fibers with few white fibers.
They respond slowly with long latency and specialized for posture
maintenance. They contain more blood capillaries, more mitochondria and
more myoglobin. They are resistant to fatigue and sensitive to hypoxia.
White muscles contain higher percentage of white fibers with few red
fibers. They respond quickly with short latency and specialized for fine skilled
movements. They contain less blood capillaries, less mitochondria and less
myoglobin. They are less sensitive to hypoxia and easily fatigued. When nerve
supply to a slow fiber is cut and replaced by nerve to a fast fiber; the slow fiber
becomes fast!
Muscle twitch is the response of a muscle to a single supra-threshold stimulus.
Strength of contraction increases with successive stimuli. Muscles that are
already contracted, contract further with additional Ca2+. If stimulation is
delivered prior to relaxation, contractions are summed. At sufficiently high
frequencies, no muscle relaxation occurs and contractions fuse into a smooth,
sustained contraction (tetanus).
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Fig: 15
Primary mechanism for increasing force of contraction is by recruitment
Tetanusof
multiple motor units at the same time and by increasing the frequency of AP at
each unit. At threshold stimulation,
first of
muscle
contraction occurs. As
Summation
twitches
stimulus intensity is increased, additional motor units are activated. Maximal
stimulus is the strongest stimulus that causes increased contraction which is
accomplished by increased neural activation.
The type of movement whether fine or gross is the function of recruitment
of numerous or few motor units respectively. When the required movement is
fine and graded; numerous small size motor units must work. When the
required movement is gross; few large size motor units can help.
Types of contraction
Muscle tension is the force of contracting muscle on an object. Load is the
reciprocal force exerted by the object. To move a load, muscle tension must be
greater than load. There are two types of contraction:
Isotonic contraction: Muscle changes in length and moves load.
Isometric contraction: Tension increases but the muscle length stays
constant. The load is greater than force e.g. maintenance of posture.
Most real-life movements involve both isometric and isotonic contraction.
Muscle Metabolism
ATP is the sole source of energy for contraction. Little ATP is stored but it is
regenerated (recycled) rapidly:
1. Direct phosphorylation of ADP by creatine phosphate
2. Anaerobic glycolysis: In the absence of oxygen, glycolytic products
(pyruvic acid) are metabolized to lactic acid producing additional small
quantities of ATP
3. Aerobic glycolysis: Provides 95% of ATP during light exercise. In presence
of oxygen, products of glycolysis are broken down entirely with the generation
of significant amounts of ATP.
4. Fatty acids are the major source of energy at rest.
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During exercise, extra-amount of oxygen is consumed to remove the excess
lactate, replenish ATP and creatine phosphate stores and to replace
myoglobin. This is called oxygen debt which is the explanation of pant.
Exhaustion is a state of fatigue due to accumulation of lactates from
anaerobic pathways resulting in decreased pH which inhibits the necessary
reactions for muscle contraction.
Length-tension relationships
Optimum resting sarcomere length (Lmax) is 2µ - 2.2µ at which maximum
tension (To) can be generated. Actin and myosin overlap such that sliding can
occur over the entire length of the actin filament. When sarcomere length is
more than Lmax; there are less actin-myosin cross bridges and muscle tension is
less than To and when sarcomere length is less than Lmax; actin filaments on
either side will overlap over each other and muscle tension is also less than To.
Abnormal contractions
Spasm: A sudden involuntary contraction of short duration.
Cramps: Painful spasmodic contraction of muscle fibers.
Convulsion: Violent tetanic contraction of entire muscle groups.
Fibrillation: Asynchronous contraction of individual muscle fibers resulting in
flutter with no effective movement.
Tic: Spasmodic twitching common in eyelid and facial muscles.
Myalgia: Pain in one or more muscles.
Myositis: Inflammation of muscle tissue.
Poliomylitis: Viral based destruction of motor neurons in the anterior horn of
the spinal cord.
Contracture: Abnormal sustained contraction resultant from continuous
availability of Ca2+ near myofibrils due to lack of Ca2+ pump back to
sarcoplasmic reticulum.
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II. Cardiac Muscle
It is branched and interdigitated and functions as syncytium due to presence
of intercalated discs and gap junctions. Its RMP is about -85 mV and its AP
is slow and characterized by presence of plateau. The AP phases are:
Phase 0: Depolarization lasts about 2 ms and occurs due activation of all Na+
channels with huge influx of Na+ ions.
Phase 1: Initial rapid repolarization occurs due fast inactivation of Na+
channels.
Phase 2: Plateau lasts about 200 ms and occurs due to opening of Ca 2+
channels and influx of Ca2+ ions.
Phase 3: Late rapid repolarization occurs due to closure of Ca2+ channels.
Phase 4: Base line (RMP)
mV
+20
1
2
0
0
3
_
85
4
0
Time
>200 ms
Pacemaker potential: Cardiac muscle contraction is myogenic (originated
inside the muscle) not neurogenic (initiated by nerve) and the nerve supply is
only regulatory. This due to the presence of specialized conductive tissue in the
heart called pacemaker tissue. This tissue has unstable low membrane
potential called prepotential or pacemaker potential which declines and
depolarizes continuously and steadily (due to slow decrease in K+ efflux)
which spreads the impulses all over the heart. Steeper prepotentials result in
tachycardia, while lower prepotentials result in bradycardia.
Prepotentials
Bradycardia
Normal rhythm
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Tachycardia
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III. Smooth muscle
Small, spindle-shaped cells arranged in sheets of opposing fibers. Generally
two sheets with fibers at right angles to each other longitudinal and circular
layers. The alternating contraction of layers results in peristalsis. Smooth
muscle lacks highly structured neuromuscular junctions and has lower myosin
to actin ratio than skeletal (1:13 vs. 1:2). It lacks troponin complex and
sarcomeres.
Electrical communication between individual smooth muscle cells (gap
junctions) make the entire sheet responds to a single stimulus. Some tissue has
pacemaker cells and some are self-excitatory.
The difference between smooth and skeletal is that Ca2+ interacts with
regulatory molecules called calmodulin not troponin. Contraction is slow,
sustained and resistant to fatigue. Smooth muscle has a unique property of
depolarization and, hence, contraction in response to stretch.
Smooth muscle also has the property of stress-relaxation (plasticity) which
means that with gradual increase in stretch; tension firstly increase and then
decrease even below its initial level. This property is of benefit especially in
uterus in order to adapt to the continuous increase in fetal size and in urinary
bladder to adapt to the continuous increase in urine volume.
Smooth muscles are in continuous state of partial contraction (tone).
Different types of nerve supply with multiple neurotransmitters are found in
smooth muscles but their role is only to modify that muscle tone. Smooth
muscle is also affected by other factors like chemicals, pH, temperature, CO 2,
O2 ....etc
Two types of smooth muscle are present:
Single-unit smooth muscle: Function as syncytium. Found mainly in the wall
of hollow viscera.
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Multi-unit smooth muscle: Has no gap junctions and each muscle works
individually. Found in the iris of eye, vas deferens, epididymus, large
pulmonary airways and large blood vessels. They have many functional
similarities to skeletal muscles but irregularly and involuntarily contract with
prolonged duration.
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Comparison of skeletal, cardiac and smooth Muscle
Characteristic
Location
Appearance
Connective
Tissue
Sarcomere
T Tubules
Gap Junctions
Neuromuscular
Junctions
Regulation of
Contraction
Skeletal
Attached to
bones, fascia and
skin
Single, long,
cylindrical,
striated,
multinucleate
Epimysium,
perimysium,
endomysium
Present
Present at each
end
None
Present
Cardiac
Walls of heart
Present
Present at one
end
Intercalated discs
None
None
None
Somatic NS;
voluntary
Autonomic NS,
intrinsic
(pacemaker),
hormones,
involuntary
SR, extracellular
fluid
Via
troponin/actin
interactions
Present
Excitation or
inhibition
Slow
Autonomic NS, hormones, local
regulation, response to stretch
Yes
In single-unit
Strength of
contraction
increases
Aerobic
Stress-relaxation response
(plasticity)
Ca2+ Source
SR
Role of Ca2+
Via
troponin/actin
interactions
None
Excitation
Pacemakers
Nervous System
Affects
Speed of
Contraction
Rhythmic
Contraction
Response to
Stretch
Respiration
Varies: slow to
fast
None
Strength of
contraction
increases
Aerobic or
anaerobic
Smooth
Single-unit: visceral organs
Multi-unit: Internal eye muscles,
large airways and arteries
Branching chains Single, non-striated, uninucleate
of cells,
uninucleate,
striated
Endomysium
Endomysium
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In single-unit
In multiunit
SR, extracellular fluid
Via calmodulin/myosin
interaction
In single-unit
Excitation or inhibition
Very slow
Primarily anaerobic