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PHYS 203 Class 1
Nervous System – master controlling and communicating system of the body
3 major functions
 sensory function
 integration
 motor function
Nervous system is divided into 2 parts
Central nervous system
 brain and spinal cord
 integrating and command centre
Peripheral nervous system
 nerves outside the CNS that extend from the brain and spinal cord
 communication lines linking the body to the CNS
Peripheral NS is further divided functionally
Sensory / Afferent Division “carry towards”
 nerve fibers that carry info from sensory receptors to the CNS
 somatic afferent fibers and visceral afferent fibers
Motor / Efferent Division “carry away”
 nerve fibers that carry info from CNS to effector organs - muscles and
glands
Motor / Efferent Division has 2 parts
Somatic Nervous System
 Voluntary Nervous System
Autonomic Nervous System
 Visceral motor nerve fibers
 Involuntary Nervous System
Cells of the Nervous System
Astrocytes (CNS)
 make exchanges between capillaries and neurons
 control chemical environment around neurons
Microglia (CNS)
 monitor health of neurons –phagocytize invading microorganisms or injured/dead neuronal
debris
Ependymal Cells (CNS)
 line central cavities of brain and spinal cord
 form a permeable barrier between the CSF and the tissue fluid in the CNS
Oligodendrocytes (CNS)
 wrap their processes around the neurons producing myelin sheath
Satellite Cells (PNS)
 surround neuron cell bodies
Schwann Cells (aka neurolemmocytes) (PNS)
 form myelin sheaths
Neurons
 conduct messages in the form of nerve impulses from one part of the body to another
 extreme longevity
 amitotic
 high metabolic rate
Cell Body
 the major biosynthetic centre of the neuron
 clusters of bodies in CNS = nuclei
 clusters of bodies in PNS = ganglia
Processes
 bundles of processes in CNS = tracts
 bundles of processes in PNS = nerves
Dendrites
 the receptive/input region
 send incoming messages toward cell body
 the signals are graded potentials not action potentials
Axon
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conducting region of the neuron
generates and transmits nerve impulses away from cell body
axolemma = axon cell membrane
axon hillock = cone shaped area of cell body where axon arises from
nerve fiber = long axon
axon collaterals = branches
terminus = axon end
terminal branches, telodendria = branches at end
axon terminals, synaptic knobs, synaptic boutons = knob-like endings at
ends of terminal branches, the secretory region for neurotransmitters
Transmission Path
impulse generated at jctn of hillock and axon (called trigger zone)
impulse along axon to axon terminals
impulse arrives at end of terminal
impulse causes stored signaling chemicals – neurotransmitters – to be released into ECF space
NT excites or inhibits other neurons or effector cells
Myelin Sheath and Neurilemma
 protects and insulates fibers
 increases nerve impulse transmission speed
 myelinated fibers – rapid nerve impulses
 unmyelinated fibres – slow nerve impulse
PNS
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schwann cells form the myelin sheath by forming concentric layers.
neurilemma – outer portion of schwann cell outside myelin sheath
nodes of Ranvier / neurofibril nodes – gaps between adjacent schwann cells, axon
collaterals emerge here
unmyelinated fibers – schwann cells form up to 15 or more recessed areas for axons,
usually thin axons
CNS
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oligodendrocytes form myelin in CNS
multiple flat processes of oligodendrocytes coil up to 60 axons at a time
Nodes of Ranvier are present but more widely spaced
White matter = regions in the brain and cord containing dense collections of
myelinated fibers
Gray matter = areas of mostly nerve cell bodies and unmyelinated fibers
PHYS 203
Class 2
Neurophysiology
 neurons are highly irritable …irritable = respond to stimuli
 neuron stimulated…..electrical impulse generated…….impulse conducted along
axon…… this response is called the Action Potential
Voltage = the measure of potential energy generated by a separated charge
Potential Difference / Potential = the voltage difference between 2 points
greater difference = higher voltage
Current = flow of electrical charge from one point to another
depends on Voltage and Resistance
Resistance = the hinderance to charge flow from substances through which the current passes
Ohm’s Law
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current = voltage / resistance
greater voltage (potential difference) = greater current
greater resistance = smaller current
plasma membranes have a slight difference in the positive and negative charges
on each side --- there is a potential across the membranes
Resting Membrane Potential
 voltage difference in the neuron vs in the extracellular fluid is -70mV
 inside is negative relative to outside
 this is called resting membrane potential and the membrane is polarized
 RMP is made from the differences in the ionic makeup of the ECF and ICF and the
diffs in membrane permeability to those ions
 cell has lower Na+ and higher K+
 ECF have higher Na+ and lower K+
 In the ECF the + Na is balanced by Cl In the ICF the + K is balanced by negative proteins
 K+ plays the most important role in determining MP
At rest membrane is:
o impermeable to negative proteins
o slightly permeable to Na
o very permeable to K
o freely permeable to Cl
at RMP the negative inside is due to greater diffusion of K+ out than Na+ into cell
Membrane Potentials that Act as Signals
change in MP produces:
o graded potentials – incoming short distance signals
o action potentials – long-distance signals along axons
Depolarization = reduction in membrane potential
inside of cell becomes less negative, closer to zero or goes above zero
Hyperpolarization = increase in membrane potential
inside of cell becomes more negative
depolarization produces nerve impulses, hyperpolarization inhibits
Graded Potentials
 short-lived
 local changes in membrane potential
 called graded because – magnitude varies directly with stim strength
 stronger stimulus – greater voltage changes - further the current flows
 triggered by a stimulus (a change in the neurons envt) casues gated ion channels
to open
 receptor potential = the graded potential created due to receptor of a sensory
neuron being excited by heat, light etc…
when depolarization occurs…..
inside the cell…….
K+ moves away from depol area and accumulates on neighbouring areas….there the K+
neutralizes the resting –ve charge
on outer membrane……
+ve ions move towards the depolarized region since the membrane charges are reversed there
and the outside is not –ve
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these +ves move and their spot becomes occupied by –ve ions (Cl, HCO3)
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therefore the outside area near the depol area becomes less positive (since the +ves
were attracted to the depol spot so they move and the –ve Cl replaces its
spot….becoming more –ve on the outside in that next spot)
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and on the inside the area becomes less negative (K+ is moving away from depol spot to
next spot making that next spot more +ve or less –ve)
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therefore that next spot is now less –ve on the inside (closer to zero)
since the inside got less negative when K+ moved towards it and the outside got more –
ve when the + moved away from it
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so that next spot is depolarized
Action Potentials
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method by which neurons send messages over long distances
AP is brief reversal of MP from -70mV to +30
depol followed by repol and usually a short hyperpol
do not decrease in strength with distance
in neurons AP also called a nerve impulse
voltage gated channels are opened at axon hillock due to a stimulus (Graded
potential) from the dendrite and cell body membranes………membrane
permeability changes
sensory neurons – AP generated by the peripheral/axonal process just proximal to
the receptor region
PHYS 203 Class 3 - Summary
Action Potential
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AP is brief reversal of memb potential with a total change in voltage of 100 mV
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from -70 to +30
Generation of AP
1. Resting State – voltage gated channels closed
2. Depolarization – increase Na permeability and reversal of memb pot
depolarization = change in memb pot from –ve to +ve
due to influx of Na+
3. Repolarization – decrease Na permeability / Increase K permeability
repolarization = return of cell to its negative state
due to Na + influx stopping
due to K+ leaving
4. Hyperpolarization – K+ permeability continues
repol has restored electrical conditions …..back to -70 but resting ionic conditions
are not restored
Na/K pump redistributes Na and K ….3 Na out, 2 K back in…more + pumped out
keeps the inside more –ve
Absolute Refractory Period – when Na+ channels are open and resetting to original state, they
will not respond to another stimulus …..ensures each AP is in an all or none event and enforces
one-way transmission of AP
Relative Refractory Period – after the ARP….most Na+ return to resting state, some K+
channels still open, repol is occurring. Threshold is higher….a stronger than normal stimulus is
needed to reopen the NA+ that have returned to normal…..therefore strong stimulus can cause
more frequent generation of APs.
Conduction Velocity
rate of propagation depends on:
axon diameter: larger = faster….due to less resistance
myelination: unmyelinated – continuous conduction
myelinated – insulates, prevents leakage of charge and allows voltage
to change fast…salutatory conduction….jumps from node to node.
type A neurons – somatic sensory and motor – skin, skel musc and joints
- largest diam, thick myelin sheath, fastest
type B neurons – ANS motor fibers, visceral sensory, small somatic sensory
- lightly myelinated, intermediate diam, medium speed
type C neurons - ANS motor fibers, visceral sensory, small somatic sensory
- unmyelinated, smallest diam, no salutatory, slowest
The Synapse – junction that mediates info transfer from one neuron to the next
Electrical Synapses
 protein channels connect cytoplasm of adjacent neurons and allow ions to flow from one
neuron to next
 good means of synchronizing activity of all interconnected neurons…..very fast
transmission
Chemical Synapses
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release and receive chemical neurotransmitters
made of: axon terminal of presynaptic neuron and receptor region for NT on
postsynaptic neuron
Synaptic Cleft separates these 2 – fluid filled space (one millionth of an inch)
nerve impulse reaches axon terminal
membrane depolarizes
Na+ channels and voltage-gated Ca++ channels open
Ca++ follows its electrochemical gradient into the terminal from ECF
Ca++ directs synaptic vesicles to fuse with axon membrane
vesicles empty contents into synaptic cleft
Ca++ is removed from the terminal…..
NT diffuses across synaptic cleft
neurotransmitter binds to protein receptors on post synaptic membrane
receptor changes shape
ion channels in membrane open
graded potential occurs
Responses at Post Synaptic neuron:
Excitatory Synapses and EPSPs
 at an excitatory synapse….NT binding causes depol of postsyn memb
 chemically gated ion channel opens…Na and K move in opposite directions
 the local graded depolarization is called EPSP
 EPSP helps trigger an AP distally at axon hillock
Inhibitory Synapses and IPSPs
 binding of NT at inhibitory synapses reduces postsyn ability to generate an AP
 induce hyperpolarization
 causes membrane to become more permeable to K+ or Cl either K+ moves out or Cl- moves in
 this is called an IPSP
Temporal Summation
 quick succession of impulses from presyn neuron…quick bursts of NT released
Spatial Summation
 large numbers of terminals stimulate the neuron at the same time
Axon hillock keeps track of the EPSPs and IPSPs, whichever dominates casues depolarization,
hyperpolarization or nothing
PHYS 203 Class 4
Neurotransmitters
 the means by which neurons communicate with each other
Classification by Chemical Structure
1 Acetylcholine - Ach
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released at neuromuscular junctions
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once released by presyn terminal, Ach binds to postsyn receptors briefly
then released and degraded to acetic acid and choline by enzyme acetylcholinesterase
located in syn cleft
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released by neurons that stimulate skel musc and some ANS neurons,
some CNS neurons release Ach too
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can be excitatory or inhibitory…..E at NMJ, I in cardiac muscle
2,Biogenic Amines
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from amino acids
1. Epinephrine
 released in motor neurons in the ANS (SNS)
 excitatory or inhibitory
2. Norepinephrine
 released in motor neurons in the ANS (SNS)
 excitatory or inhibitory
3. Dopamine
 released by substantia nigra in basal ganglia (motor control, cognition)
 excitatory or inhibitory
4. Serotonin
 secreted by brain stem
 inhibitory
 role in mood, attention, sleep, appetite
3. Amino Acids
1. Glycine
 in spinal cord
 inhibitory
2. GABA
 in spinal cord, cerebellum, hypothalamus, cortex
 inhibitory
3. Glutamate
 in spinal cord, brain stem, cortex
 excitatory
4. Peptides
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neuropeptides are strings of amino acids
1. Substance P
mediates pain signals
2. Endorphins
natural opiates…
reduce perception of pain
inhibitory – inhibits action of substance P
Sensory Receptors
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respond to changes in their environment – stimuli
Adaptation
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change in sensitivity in presence of a constant stimulus
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Phasic Receptors
fast adapting
pacinian and meissners
quickly ignore stimulus
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Tonic Receptors
sustained response..little or no adaptation
nociceptors, proprioceptors …protective importance of their information
continue to fire continuously
Receptors grouped according to Stimulus Type
1. Mechanoreceptors – stimulated by touch, pressure, vibration, stretch
2. Thermoreceptors – stim by temp changes
3. Photoreceptors – respond to light energy….retina
4. Chemoreceptors – respond to chemicals in solution
5. Nociceptors – respond to damaging stimuli that result in pain
Unencapsulated Dendritic endings/free/naked nerve endings
1. Merkel discs
 free nerve endings associated with large epidermal cells (Merkel cells) – lie in
deeper layers of epidermis…function as light touch receptors
 tonic – slow adapting
 discriminative touch
2. Root Hair Plexuses / Hair Follicle Receptors
 free nerve endings that wrap around hair follicles…light touch receptors……detect
bending of hairs…detect mosquito landing on skin…tickle
Encapsulated
1. Meissner’s Corpuscles
 just beneath epidermis in dermal papillae
 numerous in sensitive and hairless areas
 for discriminative touch
 phasic…. rapid adapting
2. Pacinian corpuscles/Lamellated Corpuscles
 deep in dermis and subcutaneous tissue under skin
 in joints, tendons, muscles
 stimulated by deep pressure, respond only when pressure is first applied or there is
a change in stimulus
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phasic
3. Ruffini Endings
 in dermis, subcutaneous tissue, joint capsules
 stimulated by deep continuous pressure
 tonic – slow adapting
Phys 203 Class 5
Proprioceptors
position sensors……….monitor position of joints, muscles
perceive :
 static body posture - static position of the body as a whole, position of body parts
 movement of body parts in relation to others……..velocity of mvmt, duration
 located in skeletal muscles, tendons, joints, ligaments, CT of bones and muscles
 advise the brain of body movements
 monitor how much the organs containing these receptors are stretched
 monitor the strength of a muscle contraction, rate of a contraction
 monitor how much tension in tendons
 monitor change in joint position
 monitor position of head relative to ground
 they are mechanoreceptors
 carry info to brain and cord
 tonic….slow-adapting
 continually monitor position of body parts and coordinate movements
Muscle Spindles
 in perimysium of muscle
 detect stretch in a muscle and initiate a reflex to resist the stretch (contract)
Anatomy of Muscle Spindle
primary sensory endings of large Type 1a fibers – innervate spindle centre
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stimulated by rate and degree of stretch
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when intrafusal fibers are stretched these sensory fibers are stretched
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depolarization occurs
secondary sensory endings of small Type II fibers – innervate spindle ends
 stimulated by degree of stretch
 detects that a stretch happened, that’s it
gamma efferent fibers - come from the spinal cord, innervate spindle ends
 maintain spindle sensitivity (cause the intrafusal fibers to contract when the extrafusal ones
are contracting so they are not slack…keeping them taut will keep them sensitive to
stretch)
alpha efferent fibers - come from the spinal cord
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stimulate the extrafusal fibers to contract
How Does the Muscle Spindle Work?
 at rest, Ia and II fibers are tonically active monitoring body position
 they are constantly firing (espec in postural muscles) and stimulating alpha motor neurons
to stimulate extrafusal fibers to contract to maintain muscle tone
 intrafusal fibres (Ia and II) get stretched as whole muscle is stretched…..Ia and II fibers fire
more rapidly than normal……stimulate alpha motor
neuron in cord…cause the
extrafusal fibers to contract and relieve the stretch
Golgi tendon organ
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in tendons
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bundles of collagen enclosed in a capsule with sensory terminals coiling around
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tendon is stretched when muscle contracts…..nerve endings are compressed and
then activated
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causes muscle relaxation and lengthening in response to tension
golgi tendon organs……..monitor the amount of tension in the muscle
muscle spindles………..monitor the length of the muscle
How does the Golgi Tendon Organ Work?
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muscle tension increases substantially during contraction
tendon is stretched
nerve endings/GTO are compressed
afferent impulses to cord
impulses to cerebellum
integration
synapse with alpha motor neurons
alpha motor neurons are inhibited
motor neurons inhibit the contracting muscle, muscle relaxes
and antagonist is activated to contract….reciprocal activation
PHYS 203 Class 6
Reflexes
Some important reflexes
a. stretch reflex
b. tendon reflex
c. flexor-withdrawal reflex
d. crossed extensor reflex
1. Stretch Reflex
 monosynaptic
 ipsilateral
 respond to muscle stretch, muscle contraction occurs
steps involved in stretch reflex
quick stretch of muscle occurs…….reflex hammer
muscle spindle is stretched
muscle spindle activated
spindle generates AP
AP travels along afferent fiber through dorsal root of spinal cord
into posterior aspect of spinal cord
synapses with an alpha motor neuron in cord….motor neuron body in anterior horn
EPSP triggered, impulse along alpha motor neuron axon
impulse arrives at NMJ, Ach released
Ach binds to extrafusal muscle cell
signals muscle AP and contraction
muscle shortens, relieves stretch
Reciprocal Inhibition
 sensory neuron synapses with an inhibitory interneuron
 inhibits the motor neuron innervating the antagonistic muscle….hamstrings
 hams will relax so that quads can contract
 antagonists then relax so they don’t resist the shortening of the stretched muscle
2. Tendon Reflex
 disynaptic
 ipsilateral
 response to muscle tension, muscle relaxation occurs
steps involved in tendon reflex
muscle tension increases substantially during contraction
tendon is stretched, nerve endings/GTO are compressed
afferent impulses to cord
integration – synapse with inhibitory interneuron
synapse with alpha motor neurons
alpha motor neurons are inhibited due to IPSP
motor neurons inhibit the contracting muscle, muscle relaxes and
antagonist is activated to contract….reciprocal activation
Reciprocal Activation
 sensory neuron synapses with another interneuron…excitatory interneuron
 that interneuron synapses with another motor neuron…causes EPSP
 antagonistic muscle contracts
so…..
with stretch reflex…EPSP to muscle to contract (quads)
IPSP to antagonist to relax it (hams)
with tendon reflex …. IPSP to muscle to relax it (quads)
EPSP to antagonist to contract it (hams)
3. Flexor Withdrawal Reflex
polysynaptic (several muscles may be involved to move limb)
 ipsilateral
 protective
 causes withdrawl of body part from painful stimulus
 EPSPs and IPSPs sent to several motor neurons….called intersegmental reflex arc
4. Crossed Extensor Reflex
polysynaptic
 contralateral
 occurs in conjunction with Flexor Withdrawal reflex in weight bearing limbs
 ipsilateral withdrawal reflex combined with a contralateral extensor reflex
 sensory neurons synapse with interneurons (EPSP and IPSP) on same side of body and
with excitatory interneuron controlling extensor muscles on opposite side of body
Assessing neuromuscular function
Dermatomes
dermatome = area of skin innervated by a single spinal nerve
 some overlapping occurs…about 50%....therefore destruction of a single spinal nerve will
not result in complete numbness anywhere
 C5-T1 supply the skin of upper limbs
 thoracic nerves supply thorax
 lumbar nerves supply anterior thighs and legs
 sacral nerves supply posterior lower legs
Myotomes
myotome = muscles supplied by motor neurons of a spinal segment
Clinical Reflexes
 show intact sensory and motor connections
Patellar Reflex - quads contract, knee extends.....tests L2 L3 L4
Achilles - gastrocs contract, ankle plantar flexes.....tests L5 S1 S2
Biceps - biceps contract, elbow flexes....tests C5 C6
Brachioradialis - brachioradialis contracts.....tests C5 C6
Triceps - triceps contract, elbow extension.....tests C7 C8
Superficial Reflexes
 elicited by gentle cutaneous stimulation
 depend on upper motor neuron pathways and spinal cord level reflex arcs
Plantar Reflex
 tests integrity of L4-S1 cord levels
 and tests the function of the corticospinal tracts (UMN paths)
 draw a blunt object along plantar surface of foot from toe to heel
 normal response – curl toes
 abnormal response – big toe dorsiflex and other toes fan out laterally (Babinski sign)
Abdominal Reflex
 tests integrity of T8-T12 cord levels
 stroke skin of lateral abdomen above to the side or below the umbilicus
 normal response – contraction of abdominal muscles causing umbilicus to move toward
stroked area
Phys Class 7
Spinal cord
function of cord:
 reflexes
 integration
 path for sensory and motor impulses
Spinal Nerves
 31 pairs
Nerve Roots
 Dorsal Root
o posterior root
o sensory fibers from periphery running into cord
o cell bodies are located at dorsal root ganglion
 Ventral Root
o anterior root
o motor fibers from brain/cord sending info to periphery
o cell bodies are inside spinal cord in anterior horn of gray matter
Organization of the Cord
Gray Matter
 neuron cell bodies of interneurons (that have synapsed with incoming sensory
neurons)
 neuron cell bodies of motor neurons (that have synapsed with interneurons or sensory
neurons)
 unmyelinated axons
 dendrites
Lateral Masses
 each lateral mass has horns – dorsal, ventral, lateral
 posterior horn
 contain cell bodies of interneurons (sensory info coming in from periphery via
dorsal horns and synapsing with interneurons cell bodies in dorsal horn (or motor
neuron bodies in the case of reflexes)
 anterior horn
 contain cell bodies of somatic motor neurons sending message out from cord
along motor nerve to muscle
Gray Commissure
 connects the lateral masses
Lateral Horns
 cell bodies of SNS motor neurons to viscera
 SNS motor axons from lateral horn join the somatic motor axons from the ventral horn
to exit out the ventral horn of the cord
Zones of Gray Matter
somatic sensory area - contains interneuron cell bodies receiving info from somatic sensory
neurons from the periphery
visceral sensory area - contains interneuron cell bodies receiving info from visceral sensory
neurons from the periphery
somatic motor area - contains cell bodies of somatic motor neurons innervating skeletal
muscles, receiving info via synapse with interneurons from brain or sensory neurons axon will
leave cord via ventral horn and run to skeletal muscle
visceral motor area - contains cell bodies of visceral motor neurons innervating viscera,
receiving info via synapse with interneurons from brain or sensory neurons axon, will
leave
cord via ventral horn and run to viscera
Phys Class 8
Spinal tracts
White Matter
ascending tracts = up = sensory info
descending tracts = down = motor info – from brain or other areas of cord
commissural tracts = transverse – across from one side of cord to other
general rules of tracts
1. All are paired – on the left and right
2. Most cross over from one side of cord to other…decussate
3. Most are chains of 2 or 3 neurons
4. Most exhibit somatotopy
Somatotopy
 spatial relationship among the tract fibers that reflects the orderly mapping of the body
ex. tracts with sensory info from the upper body lie lateral to tracts with info from the
lower body
Ascending Tracts
3 main ascending pathways
1. Nonspecific
 formed by lateral spinothalamic and anterior spinothalamic tracts
 cross over occurs in spinal cord
 pain, temp, coarse touch – sensations we are aware of but have difficulty localizing
precisely on the body surface
 anterior spinothalamic – crude touch and pressure
 lateral spinothalamic – pain and temperature
 info goes to somatosensory cortex to give conscious awareness of sensation
 lesion – loss of pain, temp, light touch on contralateral side below level of lesion
2. Specific
 mediate precise transmission of inputs from a single type of sensory receptor that can
be localized precisely on the body surface
 discriminative touch, vibration, proprioception, fine touch
 fasciculus gracilis – info from lower body…..below T6 … to medulla
 fasciculus cuneatus – info from upper body….above T6 … to medulla
 the medial leminiscus – medulla to thalamus
 info crosses at medulla
 info then goes to somatosensory cortex on contralateral side
 lesion – loss of poprioception, discriminative touch ipsilaterally below lesion (because
crossover is in the brain)
3. Spinocerebellar
 anterior
 posterior
 proprioception info from lower limbs and trunk to cerebellum (motor coordination, fine
tune motor movements)…..info from muscle spindles, GTO
 coordinates skeletal muscle activity ipsilaterally
 posterior does not decussate
 anterior decussates twice – at cord and pons
 lesion – poor coordination ipsilaterally, awkward posture and gait
nonspecific pathway
o temperature receptor
o 1st order sensory neuron enters dorsal horn of cord
o synapses with 2nd order interneuron
o crosses to other side of cord and from dorsal to anterior
o ascends cord via spinothalamic tract (anterior or lateral)
o synapse in thalamus with 3rd order interneuron
o travels to somatosensory cortex
specific pathway
o touch receptor
o 1st order sensory neuron enters dorsal horn of cord
o ascends cord via gracilis (lower body) or cuneatus (upper body)
o synapse in medulla with 2nd order interneuron
o interneuron crosses to other side
o travels to thalamus via medial leminiscal tract
o synapse with 3rd order interneuron
o travels to somatosensory cortex
spinocerebellar pathway
o muscle spindle
o 1st order sensory neuron enters dorsal horn of cord
o synapse with 2nd order neuron
o ascends to cerebellum
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efferent impulses from brain to cord
direct pathways – pyramidal tracts
indirect pathways – all others
pathways involve 2 neurons…..an upper motor neuron and a lower motor neuron
 upper motor neurons:
pyramidal cells of motor cortex
subcortical motor nuclei
 lower motor neurons:
anterior motor horn nulei
UMN = neuron above the synapse
LMN = neuron below the synapse
Direct Pathways
 aka Pyramidal tracts , aka corticospinal tracts
 voluntary muscle activity
 from pyramidal neurons in the primary motor cortex
 called direct because the axons descend without synapsing from cortex to cord
 synapse with :
interneurons that influence motor neurons
directly with anterior horn motor neurons
 anterior horn neuron stimulated….causes activation of skeletal muscle
 lateral corticospinal crosses over at medulla then continues down cord to synapse with
anterior horn motor neuron then exit to periphery
 anterior corticospinal crosses at spinal cord level at where they synapse with anterior horn
motor neuron and then exit to periphery
Indirect Pathways
 aka Extrapyramidal Tracts (“extra to”/indirect/multineuronal)
 programmed automatic movements , maintain skeletal muscle tone, balance, posture,
visual/auditory tracking, coordinate body movements
rubrospinal
 controls muscle tone – distal limb flexor muscles
 from red nuclei of midbrain
 fibers cross just below red nuclei
 down lateral columns
reticulospinal
 controls cardiovascular and respiratory regulation, muscle tone, many basic functions such as
sleep, eating
 from reticular formation in pons and medulla
 motor impulses to muscles controlling muscle tone, visceral functions
 has crossed and uncrossed fibers
 cardiovascular/respiratory viscera sends sensory info to reticular formation in pons and
medulla (brain stem), synapse with efferent interneurons that travel down reticulospinal tract,
may or may not cross over, synapse with an anterior horn motor neuron which exits the cord to
stimulate cardiovascular or respiratory viscera
tectospinal
 visual and auditory reflexes, coordinates movement of eyes/head to visual input
 in anterior white columns
 from superior colluliculi of midbrain (visual reflex centre)
 visual/auditory stimuli sends sensory info into superior colliculus in midbrain, synapse with
efferent interneurons that travel down tectospinal tract, cross over in the cord, synapse with an
anterior horn motor neuron which exits the cord to stimulate skeletal muscle
vestibulospinal
 balance, maintain muscle tone, activate limb and trunk extensors
 anterior white columns
 from vestibular nuclei of medulla
 do not cross
 vestibular labyrinth in inner ear sends impulses along cranial nerve 8 to vestibular nuclei in
medulla (info about balance), synapse with efferent interneurons, impulses then travel along
interneurons down vestibulospinal tract to synapse with anterior horn motor neuron, which
exits the cord to stimulate muscles to maintain muscle tone, balance etc.
Upper Motor Neuron Disorders
 spastic paralysis- spinal motor neurons are intact, muscles are stimulated irregularly
by spinal reflexes…muscles remain healthy longer but the movements are no longer
voluntary….they are spastic…the muscles become permanently shortened
 CP, brain injuries, spinal cord injuries, MS, stroke
 hyperreflexia
Lower Motor Neuron Disorders
 message sent from brain but motor neurons innervating muscle are absent
 flaccid paralysis
 hyporeflexia
 atrophy
Descending Tract Diseases
ALS
 motor neuron disease – UMN and LMN
 destruction of ventral horn motor neurons and pyramidal tracts
 lose muscle tone and ability, lose speak, swallow…..
 die within 5 years
 cause unknown
Polio
 destruction of ventral horn motor neurons by poliovirus
 LMN disorder
 paralysis and atrophy
 recovered survivors may experience lethargy, burning pain, weakness, atrophy…postpolio
syndrome
Phys 203 Class 9
The Brain
basic divisions:
1. cerebral hemispheres – cortex (motor, sensory, association areas), white matter, basal ganglia
2. diencephalon – hypothalamus, thalamus, epithalamus
3. brain stem- midbrain, pons and medulla
4. cerebellum
Ventricles
 continuous with central canal of cord
 hollow chambers filled with CSF, lined by ependymal cells
 lateral ventricles – in each cerebral hemisphere
 third ventricle – narrow, in diencephalons
 fourth ventricle – in hindbrain behind pons and medulla
Cerebral Hemispheres
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superior part of brain
elevated ridges = gyri
shallow grooves = sulci
deep grooves = fissures
lobes: frontal, parietal, temporal, occipital, insula (under temporal)
Cerebral Cortex
 conscious mind, awareness, communication, memory, comprehension, voluntary
movements
 brain is mapped by function: specific motor areas, specific sensory areas, association
areas, other areas for memory, language etc…
 all neurons are interneurons, not sensory or motor (the info is sensory or motor)
 each hemisphere controls opposite side of body
 the hemis are not equal in function – lateralization/specialization of cortical functions
Motor Areas
1. Primary (somatic) motor cortex 4
 precentral gyrus
 pyramidal cells (large neurons) axons form the pyramidal/corticospinal tracts, run down
cord to control voluntary movements
 motor homunculus – diagram showing the relative amount of cortical tissue devoted to
each function…areas of precise motor control (face, tongue, hands) have more neurons
devoted to them and are larger represented
2. Premotor Cortex 6
 anterior to precentral gyrus
 controls learned motor skills of a repetitive or patterned nature ex. playing instrument
 coordinates several muscle groups by activating primary motor cortex
 informs primary motor area of what motor neurons to activate to perform certain
movements
3. Broca’s area
 anterior to premotor cortex
 motor speech area – directs muscles involved in speech production
 controls movement of tongue, lips etc…
 lesion here = motor aphasia - loss of ability to produce language
 Wernickes area - processing of language
 lesion here – sensory aphasia - ability to speak is fine but use incorrect words
damage area of primary motor cortex – paralysis of muscle controlled by the specific
area...loss of voluntary mvmt, reflexes are ok
damage to premotor cortex – loss of the motor skill in that corresponding region, muscle
strength is ok. ex. typing speed would decrease, you can still make those specific type of
movements but the skill can be reprogrammed into another set of premotor neurons with practice
just like the initial learning process.
Sensory Areas
1. Primary somatosensory cortex
 postcentral gyrus of parietal lobe
 receive info from somatic sensory receptors , proprioceptors
 neurons being stimulated reflect the body region being stimulated
 somatosensory homunculus – diagram showing amount of sensory cortex devoted to a
particular body region based on that region’s sensitivity
2. Somatosensory association cortex
 posterior to primary somatosensory cortex
 integrate sensory inputs from primary sensory cortex, to produce an understanding of
what the stimulus is – size, texture, etc.
 draws upon memories of past sensory experiences
3. Visual Areas
 primary visual cortex
o posterior tip of occipital lobe
o info from retina
o somatotopy – areas in visual field are systematically organized on visual cortex left visual field is on right visual cortex and right on left, sup and info opposite
also
 visual association areas
o covers much of the occipital lobe
o uses past visual experience to interpret visual stimuli allowing recognition and
appreciation of what is being seen
o prosapagnosia – inability to recognize faces
4. Auditory Areas
 primary auditory cortex
o info from hearing receptors in ear, interpret pitch loudness, location
 auditory association areas
o perception of sound that we hear…speech, thunder etc..
o memories of sound help interpret what is heard
5. Olfactory Cortex
 info from receptors in superior nasal cavities, conscious awareness of odors
 has connections to memory and emotion….connected to smells/part of limbic system
6. Gustatory Cortex
 insula (deep to temporal lobe)
 perception of taste stimuli
PHYS 203 Class 10
Brain II
Association areas
 areas that receive inputs from many senses and send outputs to many areas
 gives meaning to info received
 stores info in memory, ties it to previous experience and knowledge
 decides what action to take
 relays info to premotor cortex
 premotor cortex communicates with primary motor cortex
1. Anterior Association area / Prefrontal Cortex
 frontal lobe
 intellect, complex learning (cognition), personality, recall
 abstract ideas, judgement, reasoning, planning
2. Posterior Association area / Gnostic Area
 temporal, parietal and occipital lobes
 interprets all sensory info of a particular situation, generates understanding of the
situation, sends info to prefrontal cortex to add emotion and intellect and determine a
response
4. Lauguage Area / Wernickes Area
 temporal lobe
 interpretation of speech
 lesion = receptive aphasia…..can hear but cant understand, can speak but words do not
make sense because they can not interpret what they are saying
5. Visceral Association
 insula
 perception of visceral stimuli
Cerebral White Matter
 communication between cerebral areas and between cortex and lower CNS areas
 commissures – connect corresponding gray areas of the 2 hemis
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corpus callosum – largest
association fibers – connect diff parts of same hemi
projection fibers – travel vertically from lower areas to cerebrum or from cortex down
internal capsule – band formed by projection fibers at top of brain stem
corona radiata – fanning/radiating of tracts above the capsule
Basal Nuclei
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caudate nucleus, putamen, globus pallidus
receive input from cerebral cortex, other subcortical nuclei
role in motor control, starting, stopping, monitoring intensity of movement
inhibit unnecessary movements, help perform several actions at once
as a group also called corpus striatum because the fibers of internal capsule pass by
them and make it look striped
Parkinsons
 destruction of substantia nigra – nuclei in midbrain that communicates with basal
ganglia to control movement
 insufficient dopamine production results in altered/reduced input to basal ganglia from
substantia nigra and motor cortex……the excitatory pathways are inhibited and the
inhibitory pathways are excited between the basal ganglia and the cortex.
 result is altered movement….rigidity, tremor, movements that should be inhibited are
not and movements that are excitatory are inhibited
Huntingtons Chorea
 mutant protein in brain cells causes neuron death….leaves holes in the brain
 inhibitory pathway of basal ganglia degenerated…thalamus no longer inhibits and
smooths the movements…….basically crossed mixed up paths and therefore jerky
uncontrolled movements
Hemiballism
 damage to subthalamic nuclei causes reduction of inhibitory output on the thalamus,
and this disinhibition gives rise to excessive excitatory drive to the cortex, which is
expressed as contralateral movements
Athetosis
 slow repetitive writing movements
Diencephalon
Thalamus
 afferent impulses from all senses synapse here for crude recognition of the stimuli
 similar impulses are relayed as a group from here via internal capsule to sensory cortex
and sensory association areas
 impulses from all areas of brain so that sensory info can be integrated and evoke the
appropriate reaction…..motor response, automatic movements…
Hypothalamus
 contains many nuclei
 visceral control centre
 vital role in homeostasis
 homeostatic roles:
1. Antonomic control centre
2. Emotional response
3. Body temperature regulation
4. Regulation of food intake
5. Regulation of water balance and thirst
6. Regulation of sleep/wake cycles
7. Control endocrine system functioning
Epithalamus
 contains pineal gland – secretes melatonin – sleep inducing signal, along with
hypothalamic nuclei regulates sleep/wake
The Brain III
Brain Stem – Mibdrain, Pons, Medulla
 produce programmed automatic survival behaviours
Midbrain
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cerebral peduncles – corticospinal/pyramidal tracts
cerebellar peduncles – tracts connecting midbrain to cerebellum
superior colliculi – visual reflex centres
inferior colliculi – auditory relay to cortex and auditory reflex
red nucleus – red…blood, iron…relay neclei in some descending motor paths that
effect limb flexion (rubrospinal)
Pons
 conduction tracts between cord and cortex and cerebellum and cortex
Medulla
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inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum
cochlear nuclei – auditory relay
vestibular nuclei – vestibular (equilibrium) relay
nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending
somatic sensory info heading to somatosensory cortex
 visceral motor nuclei:
cardiovascular centre - cardiac centre (HR), vasomotor (BP)
respiratory centre - control rate and depth of breathing
other centres - hiccupping, swallowing, coughing, sneezing
hypothalamus controls visceral functions by relaying its instructions through
medullary centres which carry them out
Cerebellum
 processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to
provide precise timing and appropriate patterns of skeletal muscle contraction for smooth
coordinated movements
 subconscious
 equilibrium inputs here to adjust posture and maintain balance
 motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary
muscle contraction
Functional Brain Systems
Limbic System
 septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus,
amygdale, hypothalamus, anterior thalamic nuclei
 emotional brain
 communicates with cerebral cortex creating relationship between feelings (limbic) and
thoughts (cortex)
Reticular Formation
 governs brain arousal
 reticular activating system – a group of neurons that send continuous impulses to
cortex…keeps cortex alert
 ascending sensory tracts synapse with RAS which enhances their arousing effect on
the cortex
 sensory inputs are filtered here
 reticulospinal tracts control skeletal muscle and some visceral motor functions
PHYS 203 Class 12
Autonomic Nervous System
Differences in somatic and autonomic NS
Effectors
 somatic – skeletal muscles
 ANS – cardiac, smooth muscle, glands
Efferent Pathways
 somatic – motor neuron bodies in CNS, axons run in spinal or cranial nerve to
skeletal muscle
 ANS – 2 neuron chain - preganglionic neuron and post ganglionic neuron
Neurotransmitter Effects
 somatic – release Ach – excitatory
 ANS – SNS and PSNS pregang neuron release Ach
SNS postgang release norepi on to the effector
PSNS postgang release Ach onto the effector
excitatory or inhibitory response depends on receptor type on effector organ
SNS and PSNS innervate the same viscera but cause opposite responses – balance
each other
SNS is generally excitatory (but not ALWAYS)
PSNS is generally inhibitory (but not ALWAYS)
Sympathetic Nervous System
 fight or flight response
 fast HR, dry mouth, cold sweaty skin, dilated pupils
 During exercise:
increase blood flow to muscles – visceral constriction of vessels
increase lung ventilation – bronchioles dilate..increases oxygen
and delivery to cells
liver releases more glucose into blood
nonessential activities are damped…GI motility slows
 SNS neurons originate from thoracolumbar areas of CNS
 preganglionic neurons synapse in sympathetic chain near spinal cord
intake
Parasympathetic Nervous System
 rest and digest state
 digestion – good idea to relax after eating….so digestion is not interfered with
by SNS activity
 keeps BP, HR, respiration rate low, high digestive rate, pupils constricted
 PSNS neurons originate from the cranial and sacral areas of CNS
 preganglionic neurons synapse in ganglia located close or in organs
Differences in SNS and PSNS
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PSNS neurons originate from brain and sacral areas of cord
SNS neurons originate from thoracolumbar areas
PSNS has long preganglionic and short postganglionic fibers
SNS has short preganglionic and long postganglionic fibers
PSNS ganglia are located in visceral effector organ
SNS ganglia are close to spinal cord
visceral sensory neurons – chemical changes, stretch, irritation of viscera
visceral reflex – receptor, sensory neuron, integration centre, motor neuron, effector
…but has 2 chain motor neuron (pregang and post gang neurons)
referred pain
since visceral pain afferents travel the same paths as somatic pain fibers… pain stimuli
arising in the viscera can be perceived as arising in somatic areas
Specific SNS functions:
1. controls vascular smooth muscle
 causes dilation or constriction of vessels
 increased tone in these muscles causes constriction of vessel… ..decreased
flow to tissue
 decreased tone in these muscles causes dilation of vessel…..increased flow to
tissue
2. thermoregulation
 SNS mediates reflexes that regulate body temp via constriction and dilation of
blood vessels
 ex. core temp increases – skin blood vessels dilate, skin is flushed with warm
blood, heat near surface of skin will radiate away from body and cool the body
 ex. core temp falls – skin vessels are constricted so that blood stays in deeper
vital organs
3. stimulates renin release in kidneys
 renin is an enzyme that promotes increase BP by acting on the kidneys to
increase water retention and therefore BP
4. Metabolic effects
 increases metabolic rate
 increases blood glucose – breakdown stored glycogen in liver
 increases lipolysis – breakdown fat to use to make ATP
Control of Autonomic Functioning
 hypothalamus is the integrative centre
 orders from there flow through lower brain centres
 cortex and limbic system can influence ex. a memory of a frightening
experience makes your heart race, thinking of food makes your mouth water
The Brain
basic divisions:
1. cerebral hemispheres - cortex, white matter, basal nuclei
2. diencephalon - thalamus, hypothalamus, epithalamus
3. brain stem - midbrain, pons and medulla
4. cerebellum
Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei
Cerebral Cortex
 awareness, communication, memory, voluntary movements
Primary (somatic) motor cortex
 control voluntary movements
Premotor Cortex
 controls learned motor skills of a repetitive or patterned nature ex. playing instrument
Broca’s area
 motor speech area – directs muscles involved in speech production
Frontal eye field
 controls voluntary movements of eyes
Primary somatosensory cortex
 receive info from somatic sensory receptors, proprioceptors
Somatosensory association cortex
 integrate sensory inputs from primary sensory cortex, to produce an understanding of
what the stimulus is – size, texture, etc.
Visual Areas
 primary visual cortex - info from retina
 visual association areas - uses past visual experience to interpret visual stimuli allowing
recognition and appreciation of what is being seen
Auditory Areas
 primary auditory cortex - info from hearing receptors in ear, interpret pitch loudness,
location
 auditory association areas - perception of sound that we hear
Olfactory Cortex
 info from receptors in superior nasal cavities
 conscious awareness of odors
Gustatory Cortex
 perception of taste stimuli
Visceral Sensory Area
 conscious perception of visceral sensations – upset stomach, full bladder
Vestibular cortex
 conscious awareness of balance
Multimodal Association areas
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areas that receive inputs from senses and send outputs to many areas
gives meaning to info received
stores info in memory, ties it to previous experience and knowledge
relays info to premotor cortex, which communicates with primary motor cortex
3 major association areas
Anterior Association area
 intellect, complex learning (cognition), personality, judgment, reasoning
Posterior Association area
 recognizing patterns, faces, localize surroundings, bind different sensory inputs into a
whole
Limbic Association area
 emotional impact
lateralization = unique abilities specific to each hemi not shared by the other
cerebral dominance = the hemisphere that is dominant for language….90% of people it is the
left…right handed
Cerebral White Matter
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communication between cerebral areas and between cortex and lower CNS areas
commissures – connect corresponding gray areas of the 2 hemis
corpus callosum – largest commissure
association fibers – connect diff parts of same hemi
projection fibers – travel vertically from to or from cortex
internal capsule – band formed by projection fibers at top of brain stem
corona radiata – fanning/radiating of tracts above the capsule
Basal Nuclei
 caudate nucleus
 putamen
 globus pallidus
 receive input from cerebral cortex and other subcortical nuclei



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some role in motor control, attention, cognition
starting, stopping, monitoring intensity of movement
inhibit unnecessary movements, help perform several actions at once
as a group also called corpus striatum because the fibers of internal capsule pass by
them and make it look striped
Diencephalon – Thalamus, Hypothalamus, Epithalamus
Thalamus
 afferent impulses from all senses synapse here
 sensory information is edited here
 crude recognition of sensation occurs here ie. pleasant or unpleasant.
Hypothalamus
 contains many nuclei for visceral control and homeostasis
 homeostatic roles:
1. Autonomic control centre - BP, HR, digestive motility, pupil size
2. Emotional response - perceives pleasure, fear, rage, acts through ANS
3. Body temperature regulation - receives input from thermoreceptors
4. Regulation of food intake - responds to blood levels of nutrients
5. Regulation of water balance and thirst - osmoreceptors
6. Regulation of sleep/wake cycles - suprechiasmatic nucleus
7. Control endocrine system functioning - releasing hormones
Epithalamus
 contains pineal gland – secretes melatonin – sleep inducing signal
Brain Stem – Mibdrain, Pons, Medulla
 produce programmed automatic survival behaviours
Midbrain





cerebral peduncles – corticospinal/pyramidal tracts
cerebellar peduncles – tracts connecting midbrain to cerebellum
superior colliculi – visual reflex centres
inferior colliculi – auditory relay to cortex and auditory reflex
red nucleus – red…blood, iron…relay neclei in some descending motor paths that
effect limb flexion (rubrospinal)
Pons
 conduction tracts between cord and cortex and cerebellum and cortex
Medulla




inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum
cochlear nuclei – auditory relay
vestibular nuclei – vestibular (equilibrium) relay
nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending
somatic sensory info heading to somatosensory cortex
 visceral motor nuclei:
cardiovascular centre - cardiac centre (HR), vasomotor (BP)
respiratory centre - control rate and depth of breathing
other centres - hiccupping, swallowing, coughing, sneezing
hypothalamus controls visceral functions by relaying its instructions through
medullary centres which carry them out
Cerebellum
 processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to
provide precise timing and appropriate patterns of skeletal muscle contraction for smooth
coordinated movements
 subconscious
 equilibrium inputs here to adjust posture and maintain balance
 motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary
muscle contraction
Functional Brain Systems
Limbic System
 septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus,
amygdale, hypothalamus, anterior thalamic nuclei
 emotional brain
 communicates with cerebral cortex creating relationship between feelings (limbic) and
thoughts (cortex)
Reticular Formation
 govern brain arousal
 reticular activating system – a group of neurons that send continuous impulses to
cortex…keeps cortex alert
 ascending sensory tracts synapse with RAS which enhances their arousing effect on
the cortex
 sensory inputs are filtered here
 reticulospinal tracts control skeletal muscle and some visceral motor functions
The Brain
1. Cerebral Hemispheres
a. Cerebral Cortex
Motor Areas:
Primary (somatic) motor cortex
Premotor Cortex
Broca’s area
Frontal eye field
Sensory Areas:
Primary somatosensory cortex
Somatosensory association cortex
Visual Areas
primary visual cortex
visual association areas
Auditory Areas
primary auditory cortex
auditory association areas
Olfactory Cortex
Gustatory Cortex
Visceral Sensory Area
Vestibular cortex
Multimodal Association areas
Anterior Association area
Posterior Association area
Limbic Association area
b. Cerebral White Matter
c. Basal Nuclei
2. Diencephalon
Thalamus.
Hypothalamus
Epithalamus
3. Brain Stem
Midbrain
Pons
Medulla
4. Cerebellum
5. Functional Brain Systems
Limbic System
Reticular Formation
The Brain
Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei
1. Cerebral Cortex
awareness, communication, memory, voluntary movements
Primary (somatic) motor cortex - control voluntary movements
Premotor Cortex - controls learned motor skills of a repetitive or patterned nature
Broca’s area - motor speech area – directs muscles involved in speech production
Primary somatosensory cortex - receives info from somatic sensory receptors, proprioceptors
Somatosensory association cortex - produces an understanding of what the stimulus is
Visual Areas
primary visual cortex - info from retina
visual association areas - uses past visual experience to interpret visual stimuli allowing
recognition and appreciation of what is being seen
Auditory Areas
primary auditory cortex - info from hearing receptors in ear - pitch loudness, location
auditory association areas - perception of sound that we hear
Olfactory Cortex
info from receptors in superior nasal cavities, conscious awareness of odors
Gustatory Cortex
perception of taste stimuli
Visceral Sensory Area
conscious perception of visceral sensations – upset stomach, full bladder
Anterior Association area / Prefrontal Cortex
intellect, complex learning (cognition), personality, judgment, reasoning
Posterior Association area / Gnostic Area
interprets all sensory info of a particular situation, generates understanding of the
situation, sends info to prefrontal cortex
Lauguage Area / Wernickes Area
interpretation of speech
Visceral Association
perception of visceral stimuli
2. Cerebral White Matter
communication between cerebral areas and between cortex and lower CNS areas
3. Basal Nuclei
caudate nucleus, putamen, globus pallidus
role in motor control, starting, stopping, monitoring intensity of movement
inhibit unnecessary movements
Diencephalon – Thalamus, Hypothalamus, Epithalamus
Thalamus
afferent impulses from all senses synapse here, sensory information is edited here
Hypothalamus
contains many nuclei for visceral control and homeostasis
1. Autonomic control centre - BP, HR, digestive motility, pupil size
2. Emotional response - perceives pleasure, fear, rage, acts through ANS
3. Body temperature regulation - receives input from thermoreceptors
4. Regulation of food intake - responds to blood levels of nutrients
5. Regulation of water balance and thirst - osmoreceptors
6. Regulation of sleep/wake cycles - suprechiasmatic nucleus
7. Control endocrine system functioning - releasing hormones
Epithalamus
contains pineal gland – secretes melatonin – sleep inducing signal
Brain Stem – Mibdrain, Pons, Medulla
produce programmed automatic survival behaviours
Midbrain





cerebral peduncles – corticospinal/pyramidal tracts
cerebellar peduncles – tracts connecting midbrain to cerebellum
superior colliculi – visual reflex centres
inferior colliculi – auditory relay to cortex and auditory reflex
red nucleus – red…blood, iron…relay neclei in some descending motor paths that
effect limb flexion (rubrospinal)
Pons
 conduction tracts between cord and cortex and cerebellum and cortex
Medulla




inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum
cochlear nuclei – auditory relay
vestibular nuclei – vestibular (equilibrium) relay
nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending
somatic sensory info heading to somatosensory cortex
 visceral motor nuclei:
cardiovascular centre - cardiac centre (HR), vasomotor (BP)
respiratory centre - control rate and depth of breathing
other centres - hiccupping, swallowing, coughing, sneezing
hypothalamus controls visceral functions by relaying its instructions through
medullary centres which carry them out
Cerebellum
provides precise timing and appropriate patterns of skeletal muscle contraction for smooth
coordinated movements, subconscious
Functional Brain Systems
Limbic System
emotional brain, communicates with cerebral cortex creating relationship between
feelings (limbic) and thoughts (cortex)
Reticular Formation
govern brain arousal, keeps cortex alert
Muscular Physiology I
Types of Muscle Tissue
1. Skeletal
2. Cardiac
3. Smooth
1. Skeletal
 striated
 voluntary
 function – body mobility
2. Cardiac
 striated
 involuntary
 function – pumps blood through heart
3. Smooth
 nonstriated
 involuntary
 function – force fluid and substances through internal body channels
Functional Characteristics
Excitability
 ability to receive and respond to stimuli (a change in environment)
Contractility
 ability to shorten forcibly when stimulated
Extensibility
 ability to be stretched
Elasticity
 ability to recoil to resting length after being stretched
Muscle Functions
1. Produces Movement
 skeletal – locomotion, manipulation
 cardiac and smooth – moves blood and other substances through heart and other
organs
2. Maintains Posture
 muscles contract to make adjustments in posture to counteract gravity
3. Stabilizes Joints
4. Generates Heat
 occurs as muscles contract, vital for maintaining body temp
Gross Anatomy
 made of muscle fibers, blood vessels, nerve fibers, connective tissue
Connective Tissue
 supports each muscle cell and reinforces the muscle as a whole
Endomysium – wraps muscle fiber
Perimysium – wraps fascicles…..groups of fibers form a fascicle
Epimysium – wraps whole muscle
Microscopic Anatomy
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plasma membrane = sarcolemma
cytoplasm = sarcoplasm
numerous granules of stored glycogen
lots of myoglobin – stores oxygen
Myofibrils
 bundles of myofilaments – actin and myosin…contractile units of the
muscle……thousands in a fiber
 sarcomeres – small sections/divisions of myofibril created due to the arrangement of
actin and myosin filaments
A band – area containing thick and thin filaments…dark band
H zone – lighter stripe in centre of A band – thick filaments only
M line – in middle of H zone – anchors the thick filaments
I band – area containing thin filaments only…light band
Z line – in middle of I band – anchors the thin filaments - protein
Sarcomere = region between 2 Z discs
 Z…I….A….H…M…H…A…I…Z
 functional unit of muscle
 arranged end to end
Thick Filament
 made of protein myosin
 myosin is made of a tail of 2 interwoven polypeptide chains and 2 flexible hinged
heads
 the heads will connect to a thin filament and swivel during muscle contraction
 each one is surrounded by 6 thin filaments
Thin Filament
 made of actin mostly
 actin is 2 intertwined long chains of connected globular units
 also in the thin filament:
tropomyosin and troponin – control the myosin interaction with
actin during a muscle contraction
Sarcoplasmic Reticulum
 elaborate smooth ER, surrounds myofibril, forms large channels at A-I junction –
terminal cisternae
 SR stores calcium and releases it when the muscle fiber is stimulated to contract
Transverse Tubules
 elongated tube of sarcolemma penetrating into cell interior at A-I jctn - AP travels deep
inside fiber, signals Ca release from terminal cisternae
Triad
 T-tubule and 2 terminal cisternae
Muscular Physiology II
Principles of Muscle Contraction
1. Filaments do not change length……..the slide
2. Z lines move closer together…..myosin pulls actin towards centre of sarcomere
3. I bands shorten
4. H zones shorten or disappear
5. A bands move closer together, they do not change length
6. zones of overlap get larger
Sliding Filament Theory - during contraction the thin filaments slide past the thick
filaments so the actin and myosin overlap to a greater degree
Steps of Muscle Contraction
1. Myosin attaches to actin
 binding site on actin is exposed, myosin head binds
 myosin head is in its high energy state, holding the potential energy that came
from breaking the bond in ATP, ADP and P remain bound to myosin head.
2. Powerstroke
 ADP and P are released from myosin….allows myosin head to move
 the potential energy that was released from the splitting of ATP is now used
and that head moves…..head changes from high energy state to low energy
state as it pulls the thin filament towards the centre of the sarcomere
3. Myosin detaches
 new ATP binds to myosin head
 myosin detaches from actin
 myosin is still in low energy state
4. Cocking of Myosin Head
 ATP is split by ATPase enzyme on myosin head…split into ADP and P
 the energy is released to put the myosin head into the high energy state
 a single powerstroke from all XBs causes 1% shortening
 muscle can shorten by 30%
Rigor Mortis - RM occurs basically because calcium is dumped into the cytoplasm
causing XBs to form but then they cannot detach because there is no ATP and therefore
do not allow relaxation of the muscle
Tropomyosin - covers myosin binding sites on actin….covered when no Ca present
Troponin - controls position of tropomyosin
Excitation Contraction Coupling - ECC is the transmission of the AP and the
subsequent sliding of the filaments
AP along motor neuron axon
axon terminal
Ach released across synaptic cleft
Ach binds to receptor on sarcolemma ot motor end plate
depolarization of sarcolemma
AP travels in all directions
AP transmission along sarcolemma and down T-tubules
terminal cisternae of SR activated to release Ca into sarcoplasm
Ca bind to troponin
troponin complex changes shape
moves tropomyosin off the binding site on actin
myosin binds to actin in its high energy state with ADP and P attached still
ADP and P are released and the head moves and pulls the actin
new ATP binds and myosin detaches in its low energy state
ATP is split to provide energy for the next powerstroke and head is cocked
Ca is constantly being taken back into SR so since AP is so brief, it does not take
long for more Ca to be taken up then is being released
not enough Ca left in sarcoplasm to bind to troponin
tropomyosin blockade forms again
troponin returns to original state
Muscular Physiology III
Review Sliding Filament steps 1-4
1. Myosin attaches to actin
 Ca++ (that was relased from SR into sarcoplasm) has already bound to troponin,
pulled tropomyosin off the binding site, myosin binds to actin
 ATP was previously split to ADP and P which are still bound to the myosin head
 myosin head is in its high energy state, holding the potential energy that came from
breaking the bond in ATP.
 myosin head is extended and waiting to move
2. Powerstroke
 ADP and P are released from myosin….allows myosin head to move
 the potential energy that was released from the splitting of ATP is now used and that
head moves…..head changes from high energy state to low energy state as it pulls the
thin filament towards the centre of the sarcomere
3. Myosin detaches
 new ATP binds to myosin head
 myosin detaches from actin
 myosin is still in low energy state
4. Cocking of Myosin Head
 ATP is split by ATPase enzyme on myosin head…split into ADP and P
 the energy is released to put the myosin head into the high energy state
back to start……
myosin binds in its high energy state with ADP and P attached still
ADP and P are released and the head moves and pulls the actin
new ATP binds and myosin detaches in its low energy state
ATP is split to provide energy for the next powerstroke and head is cocked
Muscle Contraction part II
 muscle cells respond all or none
 each cell contracts fully but since a muscle is made of tons of cells the whole muscle
contraction can vary in force and duration
 depends on # fibers contracting simultaneously
The Motor Unit
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MU is the nerve-muscle functional unit
MU is a motor neuron and all the muscle fibers it innervates
motor nerve is made of tons….hundreds of neurons
neuron axons enter the muscle and branch and form NMJs with muscle fibers
motor neuron will fire and all the muscle fibers it innervates will contract
a MU may have 4-100 or more muscle fibers in the MU
small MU = 4 muscle fibers served by one neuron…fine motor control…fingers, eyes
large MU = 100 – less precise movements
fibers of a MU are not clustered, they are spread through the muscle……stim of a MU
causes weak contraction of entire muscle
Muscle Twitch
twitch = response of a motor unit to a single action potential
contraction response …..contract fast then relax
3 phases
1. Latent
 few msec following stim
 ECC is occurring….AP along sarcolemma, Ttubule, calcium release, troponin…XBs
starting to move
 muscle tension increasing but no response on myogram
2. Contraction
 XBs active
 if tension is great enough to overcome the load, the muscle will shorten
3. Relaxation
 calcium reuptake into SR
 muscle no longer contracting
 some twitch responses are fast and brief – eye muscles
 some are slow and contract longer – soleus, gastros
 diffs reflect metabolic properties and enzyme diffs
Graded Response of Muscle Twitch
 muscles do not normally twitch….see in lab and in some neuromusc probs
 contractions are smooth and vary in strength as diff demands are placed on them
graded muscle response = the variations in contraction strength to ensure proper control of
muscle movement
ex. allows the same muscles to …..pick up baby, crush pop can…..diff amt of strength needed for
different activity
can be graded by:
 changing frequency of stimulation
 changing strength of stimulus (#MUs activated)
Changing Stimulation Frequency
 increase firing rate = increase muscular force
 a second electrical stimulation delivered very soon after first…rides on shoulders of
first twitch…………wave summation
 second contraction occurs before muscle has completely relaxed
 more calcium is being released from SR while some is still present from the last
contraction not yet reuptaken so more Ca is floating..… tension produced in second
contraction produces more shortening than the first …….contractions are summed
 absolute refractory period is always honored
 if stim faster and faster…less relaxation time between twitches…….Ca concentration in
sarcoplasm increases more and more and summation is greater and
greater………..eventually max tension reached, no relaxation between twitches
……smooth contraction…..tetanus
Stronger Stimuli
 recruitment controls force of contraction
 multiple motor unit summation
 activating a large number of MUs = increase in muscular force
 size principle…..small muscle fibers are controlled by small highly excitable motor
neurons……activated first
 as contractile strength increases….recruit larger MUs containing larger muscle
fibers….large neurons are less excitable…higher threshold, recruited later
 size principle allows force increases to occur in small steps
 all MUs can be activated at same time but usually not
Muscle Tone
 skel muscles almost always are slightly contracted----muscle tone
 due to stretch receptors that are always sensitive to even small amounts of stretch in
monitoring posture
 tone keeps muscles firm and ready to respond to stimulation…ie. primed and ready to
go
 tone stabilizes joints and maintains posture
Muscle Tension – the force generated by a contracting muscle on an object
Muscle Contraction – activation of myosin cross bridges
Isotonic Contraction - same/constant tension
 once sufficient tension has been generated to move a load the tension generally
remains constant
 muscle will change length to move the load
concentric – shortens to do work
eccentric – generates force while lengthening
50% more forceful than CON
more DOMS
stretching during the contraction causes microtears
ex. squat – bend….quads are stretching and contracting to control the movement (muscle
braking) and prevent joint injury
stand back up…concentric contract quads as they shorten and knees extend
ECC contraction can be intentional for strengthening..pilates curl back…or ECC can be seen in
the controlling part of a CON mvmt.
ECC is stronger..you can curl in a bicep curl…when that is too heavy to CON contract you will still
be able to ECC contract to put it down
Isometric contraction – same length
 muscle attempts to move a load greater than the force/tension the muscle is able to
develop
 maintenance of posture is isometric or holding joints stable while movement occurs at
other muscles…ex.sit up……..neck muscle are working to hold neck stable
 ex. in squat….pause in bent position…..quads contracting isometrically to hold knees
stable…their tension will exceed the load and then the contraction in CON
so squat……ECC…ISO…CON
at same time …..ISO of lumbar muscles
isotonic…..thin filaments are sliding
isometric…XBs are generating force but are not moving the thin filaments “spinning their wheels
on the same actin binding sites”
Factors affecting Muscle Contraction
1. Recruitment
2. Hypertrophy
3. Series Elastic Components
4. Degree of Muscle Stretch
1. Recruitment
more motor units recruited = greater force generated
2. Hypertrophy
size of muscle fiber
bulkier fiber = more tension developed = more strength
larger muscles have larger muscle cells with more myofibrils with more actin and myosin
3. Elastic Elements
series elastic components are non-contractile components of muscle….fascia
XBs initially pull the fascia taut (internal tension) and no actual muscle movement is seen
once that is taut it pulls through to the ends of the muscle/bone and causes movement
(external tension)
time is required to take up this slack and stretch that fascia
when a muscle is stimulated rapidly the series elastic component is already taken up so
there is no time needed for that
4. Degree of Muscle Stretch
 muscle has an optimal resting length…length at which muscle can generate maximum
force
 ideal length-tension relationship --- ideal length where the optimal amt of tension can
be developed
 ideal – muscle is slightly stretched and thick and thin overlap optimally – permits sliding
along nearly the whole filament
 if too stretched – no overlap…myosin heads can not attach to myosin
 too much overlap – sarcomere is cramped, think filaments touch and interfere with one
another, no further shortening can occur
 optimal length – 80%-120% of resting length
 joint structure usually prevents movement outside this range
Factors Affecting Velocity and Duration of Contraction
1. Load placed on the muscle
2. Muscle Fiber Type
1. Load - resistance
heavier load = slower contraction (slower velocity)
heavier load = fatigue faster
heavier load = shorter duration of contraction (shorter duration)
lighter load = faster contraction (faster velocity)
lighter load = longer to fatigue
lighter load = longer duration of contraction possible (longer duration)
larger load
 longer latent period
latent period is when that AP is traveling through Ttubules to
myofibrils….when motor units are being activated…if the load is heavier, more
MUs are trying to be activated
 slower contraction (slower velocity)
 shorter duration of contraction (shorter duration)
too large load
 muscle cant move the load – isometric
 velocity = zero
2. Fiber Type
 different fiber types increase or decrease velocity of contraction
 different fiber types increase or decrease duration of contraction
Fibers are classified based on:
Speed of Contraction
ATP formation pathway
1. Speed of contraction
slow – slow splitting ATPase on the myosin and slower pattern of electrical activity of their motor
neuron
fast – fast splitting ATPase on the myosin and slower pattern of electrical activity of their motor
neuron
fast
medium
slow
2. ATP formation pathway
oxidative fibers – use aerobic pathways
glycolytic fibers – use anaerobic pathways
slow oxidative
fast oxidative
fast glycolytic
Fast Glycolytic
 fast ATPase
 quick neuron stimulus-response
 use anaerobic glycolysis
 few mitochondria – not needed since don’t use O2 to make ATP
 few capillaries – don’t need to exchange as much O2
 low myoglobin – don’t need to store as much O2
 high glycogen storage – use glycogen for fuel
 quick to fatigue – produce lactic acid and run out of ATP since produce only small
amounts, run out of glycogen reserves
 large fibers - don’t depend on continuous nutrient and O2 diffusion from blood so the
cell can be larger
 generate lots of power – due to large size and therefore lots of myofibrils/filaments
 good for : short term, rapid, intense movments
Slow Oxidative
 slow ATPase
 slow neuron-stimulus response
 uses aerobic respiration
 many mitochondria – for ATP production in krebs and ETC
 lots of capillaries – need O2 to make ATP
 lots of myoglobin – need O2 to make ATP
 low glycogen storage – does not use it for ATP
 fatigue-resistant – don’t produce lactic acid, don’t run out of ATP fast
 small fibers – must be small to be in close contact with capillaries
 generate little power – due to small size, fewer fibrils and filaments
 good for : endurance
Fast Oxidative Fibers
 intermediate fibers
 mixture of features of FG and SO
 fast ATPase
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uses aerobic respiration
many mitochondria
lots of capillaries
high myoglobin
intermediate levels of stored glycogen
moderately fatigue-resistant
intermediate size
 most muscles are made of a mixture of all types….allows muscles to have a range of
contractile speeds
 genetically determined
 can alter with type of training…..strength vs endurance training
Muscular Physiology IV
Muscle Metabolism
ATP used for:
 XB movement…..ATPase breaks ATP to ADP and P and releases energy stored in
the bonds…this puts myosin head into high energy state ready to pivot
 myosin head detachment – when ATP binds myosin head detaches
 calcium pump – active pump for Ca back into SR
ATP
 limited stores
 enough for 4-6 seconds
 must be regenerated fast
ATP is formed by:
1. interaction ADP with creatine phosphate
2. from stored glycogen via glycolysis
3. aerobic respiration
1. Phosphorylation of ADP by creatine phosphate
 CP is a high energy molecule stored in muscle
 CP transfers its P to ADP to make ATP and creatine
 occurs fast while other ATP pathways are firing up
 very quick and efficient
 catalyzed by creatine kinase
 stored ATP and CP provide 10-15 sec of max muscle power
2. Glycolysis
 use glucose from blood or use glycogen stores from muscle
 glycolysis----2 pyruvic acid made…..2 ATP made
 if O2 present….pyruvic acid enter mitochondria…..krebs….ETC
 if O2 absent …heavy fast contraction..muscles bulge and compress blood vessels
 PA makes LA
 LA enters blood goes to liver, heart, kidney….used as energy source
 liver cells can change it to glucose or PA to be used again to make ATP
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Aerobic
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makes less ATP than the aerobic path
makes ATP faster than aerobic path
good for 30-40 sec of strenuous activity
CP and anaerobic provide ATP for about 1 min of strenuous muscle activity
but lots of glucose used to make small amount of ATP
lots of LA produced….fatigue
during rest and light-mod activity
in mitoch
uses O2
energy is released and transferred and captured in ATP bonds
initially glycogen and glucose are used for the first 30 min
then fatty acids are used
36/38ATP are made per glucose
but its slow
Energy Systems used during activity
 if enough O2 present…ATP made aerobically…..light –mod activity can continue for
several hours
 if demands on muscle increase….need ATP faster….glycolysis begins to contribute
aerobic endurance – length of time a muscle can continue to contract using aerobic pathways
anaerobic threshold – point where anaerobic metab kicks in
 weight lifting, diving, sprinting…surge of power for few sec…ATP and CP
 tennis, soccer, 100 meter swim…….glycolysis
 marathon…aerobic
Muscle Fatigue
 physiological inability to contract…muscle may still be receiving stimuli
 psychological fatigue….muscles can still contract but we feel tired
 prob with ECC coupling
 lack of ATP does not cause fatigue….lack of ATP causes contractures/rigor mortis
 lactic acid accumulates, alters contractile proteins..causes that ache and burn
feeling….but has more effect on central/psychological fatigue…does not
physiologically limit….body regulates the H well
 during AP transmission, K+ is lost from muscle cells…disturbs membrane
potential…alters calcium release from SR
 P accumulates when CP and ATP breakdown…P interferes with calcium release
basically short duration intense activity……ionic disturbances alter EC coupling
long duration low intensity exercise…damages SR..interferes with Ca release
Oxygen Debt
exercise causes:
 lactic acid accumulation….must be converted to pyruvic acid
 glycogen depletion….must be replenished
 ATP depleted…..stores must be replaced
 CP depleted…..stores must be replaces
all of these require oxygen…..does not happen in anaerobic exercise
so these activities are deferred until O2 available….O2 debt is incurred
oxygen debt = the extra amount of oxygen the body must take in for the restorative processes
 repay debt…….by heavy breathing
 lactic acid accumulates in blood…the H will leave the lactic acid enters blood
 high H in blood…..low pH
 high CO2 in blood triggers heavy breathing…..
 try to eliminate CO2 which frees up HCO3 so the H can bind to it to form carbonic
acid… a weak safe acid used as an intermediate molecule controlling respiration
Muscle Pathologies
Myasthenia Gravis
 autoimmune….immune system attacks own body
 antibodies attack Ach receptors at NMJ
 signal not transmitted
 muscle weakness, paralysis, death possible
Muscular Dystrophy
 affected muscles initially enlarge due to fat and CT deposit but muscle fibers atrophy
and degenerate
Duchenne MD
 X linked recessive….females carry it, usually affects boys
 muscles weaken….limbs first then progresses upwards
 death in 20s…respiratory failure
 muscle fibers lack dystrophin….strengthening protein that stabilizes the
sarcolemma….therefore the sarcolemma tears during contraction..excess calcium
enters cell…upsets homeostasis…damages actin and myosin and inflammatory cells
accumulate in surrounding CT……the regenerative capacity of the muscle is
lost….damages cells die…loss of muscle mass
Smooth Muscle
 found in walls of hollow organs and blood vessels
fibers:
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spindle shape
small
single nucleus
gap junctions – specialixed groups of cells that connect adjacent cells to
the AP from cell to cell
arranged in sheets
transmit
layers:
longitudinal layer – fibers run parallel to long axis of organ….contraction
of these causes organ to dilate and shorten
circular layer – fibers run around the circumference of the
organ…contraction of this layer constricts the lumen and elongates
the organ
 alternating contraction and relaxation of these layers mixes substances in lumen and
squeezes contents through organ’s internal pathway…peristalsis
functions:
1. moves substances…blood, peristalsis
2. expels contents….bile from gallbladder, urine from bladder
3. guards entrances and exits
Structure:
1. no NMJ – NT releases from bulbous swellings on ends of ANS motor fibers into a wide
synaptic cleft area
2. no T tubules – sarcolemma has different pouchlike infoldings (caveolae) of ECF and Ca
3. Ca enters from ECF through sarcolemma wall of inpouching
Organization:
1. nonstriated, no sarcomeres
2. thick filaments are different – longer
3. filaments arranged in bundles, not sarcomeres
4. more actin per myosin
5. myosin heads along whole length..more XBs
6. powerful contractions
7. have tpopomyosin, no troponin
8. no z discs…have dense bodies…collections of cytoskeleton protein that anchor the
cells..sliding of filaments pulls on this network
contraction…areas of sarcolemma between the dense bodies network bulge…looks puffy
RECALL…..FROM SEMESTER 1….
Glycolysis – use glucose to make pyruvic acid to fuel krebs cycle
from 1 molecule of glucose:
2 ATP used
4 ATP made
2 NADH2 carrying H to be used later in ETC to make ATP
2 pyruvic acid
****result is 2 ATP and 2 NADH2 which will produce 6 ATP
Pyruvic acid
if no O2 present: Lactic Acid formed when the NADH gives off the H…
the H joins the pyruvate to make lactic acid… the NADH2 needs to
dump off the H and return to NAD to be used in glycolysis so
glycolysis can continue
if O2 present……pyruvic acid..to Krebs
Krebs - when O2 is present, use pyruvic acid to fuel the krebs reactions to create NADH2
and FADH2 which will ultimately make ATP
one pyruvic acid enters mitochondria:
3 carbons removed……3 CO2 made (1 before and 2 during krebs)
1 FADH2 created in Krebs
4 NADH2 created (1 before and 3 in krebs)
1 ATP created
recall one glucose makes 2 pyruvic acid so
6 CO2
2 FADH2
8 NADH2
2 ATP
****result is 2ATP, 2 FADH2 which will produce 4 ATP, 8 NADH2 which will produce 24 ATP
ETC – oxidize NADH2 and FADH2 (remove the H) so that glycolysis and krebs can
continue…(glycolysis and krebs can only continue if NAD and FAD are available to pick up more
H)…and so electrons transferred in the process can be captured by ATP synthase to make ATP
each NADH2 that transfers H2 to the ETC contributes enough energy to make 3 ATP
each FADH2 starts a little farther along so contributes less energy so 2 ATP are made
SO……
glycolysis – 1 molecule of glucose
2 ATP made (4 made, 2 used)
2 NADH2
2 pyruvic acid
krebs – 2 pyruvic acid
6 CO2
2 FADH2
8 NADH2
2 ATP
ETC
2 NADH from glycolysis = 6 ATP
8 NADH from Krebs = 24 ATP
2 FADH from Krebs = 4 ATP
end result….
1 glucose molecule turns into CO2 and H2O and 38** ATP are created
glycolysis
ETC
2 ATP ……………………………….…………………………….….…2
2 NADH
……………………………..…6 ATP**……………….. 6
total ATP
krebs
2 ATP ……………………………….…………………………………..2
8 NADH………………………………………24 ATP……………..…24
2 FADH……………………………………….4 ATP ………………….4
total = 38 ATP
** but the 2NADH made during glycolysis cannot enter the mitochondria easily….uses 2 ATP for
transport so only 2 ATP are created from each NADH so 4 instead of 6……so 38 minus 2 = 36
Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying
degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia
gravis, which is Latin and Greek in origin, literally means "grave muscle weakness." With current
therapies, however, most cases of myasthenia gravis are not as "grave" as the name implies. In
fact, for the majority of individuals with myasthenia gravis, life expectancy is not lessened by the
disorder.
The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity
and improves after periods of rest. Certain muscles such as those that control eye and eyelid
movement, facial expression, chewing, talking, and swallowing are often, but not always, involved
in the disorder. The muscles that control breathing and neck and limb movements may also be
affected.
What causes myasthenia gravis?
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It
occurs when normal communication between the nerve and muscle is interrupted at the
neuromuscular junction - the place where nerve cells connect with the muscles they control.
Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter
substance called acetylcholine. Acetylcholine travels through the neuromuscular junction and
binds to acetylcholine receptors which are activated and generate a muscle contraction.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the
neuromuscular junction which prevents the muscle contraction from occurring. These antibodies
are produced by the body's own immune system. Thus, myasthenia gravis is an autoimmune
disease because the immune system - which normally protects the body from foreign organisms mistakenly attacks itself.
What are the symptoms of myasthenia gravis?
Although myasthenia gravis may affect any voluntary muscle, muscles that control eye and eyelid
movement, facial expression, and swallowing are most frequently affected. The onset of the
disorder may be sudden. Symptoms often are not immediately recognized as myasthenia gravis.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in
swallowing and slurred speech may be the first signs. The degree of muscle weakness involved
in myasthenia gravis varies greatly among patients, ranging from a localized form, limited to eye
muscles (ocular myasthenia), to a severe or generalized form in which many muscles sometimes including those that control breathing - are affected. Symptoms, which vary in type
and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision
(diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait,
weakness in arms, hands, fingers, legs, and neck, a change in facial expression, difficulty in
swallowing and shortness of breath, and impaired speech (dysarthria).
The Brain
basic divisions:
1. cerebral hemispheres - cortex, white matter, basal nuclei
2. diencephalon - thalamus, hypothalamus, epithalamus
3. brain stem - midbrain, pons and medulla
4. cerebellum
Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei
Cerebral Cortex
 awareness, communication, memory, voluntary movements
Primary (somatic) motor cortex
 control voluntary movements
Premotor Cortex
 controls learned motor skills of a repetitive or patterned nature ex. playing instrument
Broca’s area
 motor speech area – directs muscles involved in speech production
Frontal eye field
 controls voluntary movements of eyes
Primary somatosensory cortex
 receive info from somatic sensory receptors, proprioceptors
Somatosensory association cortex
 integrate sensory inputs from primary sensory cortex, to produce an understanding of
what the stimulus is – size, texture, etc.
Visual Areas
 primary visual cortex - info from retina
 visual association areas - uses past visual experience to interpret visual stimuli allowing
recognition and appreciation of what is being seen
Auditory Areas
 primary auditory cortex - info from hearing receptors in ear, interpret pitch loudness,
location
 auditory association areas - perception of sound that we hear
Olfactory Cortex
 info from receptors in superior nasal cavities
 conscious awareness of odors
Gustatory Cortex
 perception of taste stimuli
Visceral Sensory Area
 conscious perception of visceral sensations – upset stomach, full bladder
Vestibular cortex
 conscious awareness of balance
Multimodal Association areas
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areas that receive inputs from senses and send outputs to many areas
gives meaning to info received
stores info in memory, ties it to previous experience and knowledge
relays info to premotor cortex, which communicates with primary motor cortex
3 major association areas
Anterior Association area
 intellect, complex learning (cognition), personality, judgment, reasoning
Posterior Association area
 recognizing patterns, faces, localize surroundings, bind different sensory inputs into a
whole
Limbic Association area
 emotional impact
lateralization = unique abilities specific to each hemi not shared by the other
cerebral dominance = the hemisphere that is dominant for language….90% of people it is the
left…right handed
Cerebral White Matter
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communication between cerebral areas and between cortex and lower CNS areas
commissures – connect corresponding gray areas of the 2 hemis
corpus callosum – largest commissure
association fibers – connect diff parts of same hemi
projection fibers – travel vertically from to or from cortex
internal capsule – band formed by projection fibers at top of brain stem
corona radiata – fanning/radiating of tracts above the capsule
Basal Nuclei
 caudate nucleus
 putamen
 globus pallidus
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receive input from cerebral cortex and other subcortical nuclei
some role in motor control, attention, cognition
starting, stopping, monitoring intensity of movement
inhibit unnecessary movements, help perform several actions at once
as a group also called corpus striatum because the fibers of internal capsule pass by
them and make it look striped
Diencephalon – Thalamus, Hypothalamus, Epithalamus
Thalamus
 afferent impulses from all senses synapse here
 sensory information is edited here
 crude recognition of sensation occurs here ie. pleasant or unpleasant.
Hypothalamus
 contains many nuclei for visceral control and homeostasis
 homeostatic roles:
1. Autonomic control centre - BP, HR, digestive motility, pupil size
2. Emotional response - perceives pleasure, fear, rage, acts through ANS
3. Body temperature regulation - receives input from thermoreceptors
4. Regulation of food intake - responds to blood levels of nutrients
5. Regulation of water balance and thirst - osmoreceptors
6. Regulation of sleep/wake cycles - suprechiasmatic nucleus
7. Control endocrine system functioning - releasing hormones
Epithalamus
 contains pineal gland – secretes melatonin – sleep inducing signal
Brain Stem – Mibdrain, Pons, Medulla
 produce programmed automatic survival behaviours
Midbrain
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cerebral peduncles – corticospinal/pyramidal tracts
cerebellar peduncles – tracts connecting midbrain to cerebellum
superior colliculi – visual reflex centres
inferior colliculi – auditory relay to cortex and auditory reflex
 red nucleus – red…blood, iron…relay neclei in some descending motor paths that
effect limb flexion (rubrospinal)
Pons
 conduction tracts between cord and cortex and cerebellum and cortex
Medulla
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inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum
cochlear nuclei – auditory relay
vestibular nuclei – vestibular (equilibrium) relay
nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending
somatic sensory info heading to somatosensory cortex
 visceral motor nuclei:
cardiovascular centre - cardiac centre (HR), vasomotor (BP)
respiratory centre - control rate and depth of breathing
other centres - hiccupping, swallowing, coughing, sneezing
hypothalamus controls visceral functions by relaying its instructions through
medullary centres which carry them out
Cerebellum
 processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to
provide precise timing and appropriate patterns of skeletal muscle contraction for smooth
coordinated movements
 subconscious
 equilibrium inputs here to adjust posture and maintain balance
 motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary
muscle contraction
Functional Brain Systems
Limbic System
 septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus,
amygdale, hypothalamus, anterior thalamic nuclei
 emotional brain
 communicates with cerebral cortex creating relationship between feelings (limbic) and
thoughts (cortex)
Reticular Formation
 govern brain arousal
 reticular activating system – a group of neurons that send continuous impulses to
cortex…keeps cortex alert
 ascending sensory tracts synapse with RAS which enhances their arousing effect on
the cortex
 sensory inputs are filtered here
 reticulospinal tracts control skeletal muscle and some visceral motor functions
The Brain
1. Cerebral Hemispheres
a. Cerebral Cortex
Motor Areas:
Primary (somatic) motor cortex
Premotor Cortex
Broca’s area
Frontal eye field
Sensory Areas:
Primary somatosensory cortex
Somatosensory association cortex
Visual Areas
primary visual cortex
visual association areas
Auditory Areas
primary auditory cortex
auditory association areas
Olfactory Cortex
Gustatory Cortex
Visceral Sensory Area
Vestibular cortex
Multimodal Association areas
Anterior Association area
Posterior Association area
Limbic Association area
b. Cerebral White Matter
c. Basal Nuclei
2. Diencephalon
Thalamus.
Hypothalamus
Epithalamus
3. Brain Stem
Midbrain
Pons
Medulla
4. Cerebellum
5. Functional Brain Systems
Limbic System
Reticular Formation
The Brain
Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei
1. Cerebral Cortex
awareness, communication, memory, voluntary movements
Primary (somatic) motor cortex - control voluntary movements
Premotor Cortex - controls learned motor skills of a repetitive or patterned nature
Broca’s area - motor speech area – directs muscles involved in speech production
Primary somatosensory cortex - receives info from somatic sensory receptors, proprioceptors
Somatosensory association cortex - produces an understanding of what the stimulus is
Visual Areas
primary visual cortex - info from retina
visual association areas - uses past visual experience to interpret visual stimuli allowing
recognition and appreciation of what is being seen
Auditory Areas
primary auditory cortex - info from hearing receptors in ear - pitch loudness, location
auditory association areas - perception of sound that we hear
Olfactory Cortex
info from receptors in superior nasal cavities, conscious awareness of odors
Gustatory Cortex
perception of taste stimuli
Visceral Sensory Area
conscious perception of visceral sensations – upset stomach, full bladder
Anterior Association area / Prefrontal Cortex
intellect, complex learning (cognition), personality, judgment, reasoning
Posterior Association area / Gnostic Area
interprets all sensory info of a particular situation, generates understanding of the
situation, sends info to prefrontal cortex
Lauguage Area / Wernickes Area
interpretation of speech
Visceral Association
perception of visceral stimuli
2. Cerebral White Matter
communication between cerebral areas and between cortex and lower CNS areas
3. Basal Nuclei
caudate nucleus, putamen, globus pallidus
role in motor control, starting, stopping, monitoring intensity of movement
inhibit unnecessary movements
Diencephalon – Thalamus, Hypothalamus, Epithalamus
Thalamus
afferent impulses from all senses synapse here, sensory information is edited here
Hypothalamus
contains many nuclei for visceral control and homeostasis
1. Autonomic control centre - BP, HR, digestive motility, pupil size
2. Emotional response - perceives pleasure, fear, rage, acts through ANS
3. Body temperature regulation - receives input from thermoreceptors
4. Regulation of food intake - responds to blood levels of nutrients
5. Regulation of water balance and thirst - osmoreceptors
6. Regulation of sleep/wake cycles - suprechiasmatic nucleus
7. Control endocrine system functioning - releasing hormones
Epithalamus
contains pineal gland – secretes melatonin – sleep inducing signal
Brain Stem – Mibdrain, Pons, Medulla
produce programmed automatic survival behaviours
Midbrain
 cerebral peduncles – corticospinal/pyramidal tracts




cerebellar peduncles – tracts connecting midbrain to cerebellum
superior colliculi – visual reflex centres
inferior colliculi – auditory relay to cortex and auditory reflex
red nucleus – red…blood, iron…relay neclei in some descending motor paths that
effect limb flexion (rubrospinal)
Pons
 conduction tracts between cord and cortex and cerebellum and cortex
Medulla




inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum
cochlear nuclei – auditory relay
vestibular nuclei – vestibular (equilibrium) relay
nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending
somatic sensory info heading to somatosensory cortex
 visceral motor nuclei:
cardiovascular centre - cardiac centre (HR), vasomotor (BP)
respiratory centre - control rate and depth of breathing
other centres - hiccupping, swallowing, coughing, sneezing
hypothalamus controls visceral functions by relaying its instructions through
medullary centres which carry them out
Cerebellum
provides precise timing and appropriate patterns of skeletal muscle contraction for smooth
coordinated movements, subconscious
Functional Brain Systems
Limbic System
emotional brain, communicates with cerebral cortex creating relationship between
feelings (limbic) and thoughts (cortex)
Reticular Formation
govern brain arousal, keeps cortex alert