BIOL B32 - Ch9 Physiology of Skeletal Muscle Fibers

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somatic motor neurons

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the nerve cells that activate skeletal muscle fibers

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somatic motor neurons reside where

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in the brain or spinal cord

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Muscular System

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75 Terms

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somatic motor neurons

the nerve cells that activate skeletal muscle fibers

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somatic motor neurons reside where

in the brain or spinal cord

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somatic is voluntary or involuntary?

voluntary

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axons

long threadlike extensions of the somatic motor neuron

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axons bundled with nerves do what

transmit action potentials to the muscle cells they serve to initiate contraction

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action potentials

electrical impulses where it is a reversal on the membrane potential (the inside of the cell becomes positive)

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when there is an electrical charge there is

potential

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resting membrane potential

the electrical charge across a membrane when a cell is at rest

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how much more negative is the intracellular environment of a resting membrane potential?

-70mV

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<p>due to the selective permeability properties of the membrane the ions…</p>

due to the selective permeability properties of the membrane the ions…

cannot freely cross and are therefore unable to reach equilibrium and active transport by the pump

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<p>high or low concentration of sodium outside the cell?</p>

high or low concentration of sodium outside the cell?

high

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<p>high or low concentration of potassium outside the cell?</p>

high or low concentration of potassium outside the cell?

low

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ligand

a chemical messenger

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<p>ligand-gated channels</p>

ligand-gated channels

open and close due to presence or absence of a ligand that binds to the receptor site

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if a ligand binds..

the channel opens and ions move

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if a ligand does not bind or is not present…

the channel closes and ions cannot move

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where are ligand-gated channels found?

the dendrites and cell body of the motor neuron, and the neuromuscular junction

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<p>voltage gated channels</p>

voltage gated channels

open and close in response to a change in voltage

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if the membrane potential reaches a certain voltage or charge

the voltage-gated channel opens

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if the membrane potential reaches a different voltage or charge

the voltage-gated channel closes

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where are voltage gated channels found?

along axons of neurons and sarcolemma of muscle fiber and act much faster compared to ligand-gated channels

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when a cell receives a signal, what happens to the ligand gated sodium channels?

the sodium channels open and sodium beings to leak into the cell down its concentration gradient

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what is the signal the cell receives to open the ligand-gated sodium channel?

the neurotransmitter binds to its receptor

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local depolarization

a step wise progression toward a more positive charge

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<p>threshold</p>

threshold

the minimum amount of depolarization required to initiate an action potential

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all or none meaning for action potential

if a threshold is achieved an action potential is fired, but if it’s not then no action potential takes place and cell returns back to its resting membrane potential

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what are the two phases of action potential?

depolarization and repolarization phase

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<p>-70mV</p>

-70mV

opening of ligand-gated sodium channels where sodium will leak in and produce a local depolarization

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<p>-65mV </p>

-65mV

threshold, the opening of voltage-gated sodium channels where massive amounts of sodium rush inside the cell which produces rapid depolarization

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<p>+30mV</p>

+30mV

closing of the voltage gated sodium channels and opening of the potassium channels where massive amounts of potassium rush out and produces rapid repolarization

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<p>-70mV</p>

-70mV

voltage gated potassium channels close and sodium/potassium pumps reestablish the concentration gradient

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<p>refractory period</p>

refractory period

a short period after an action potential has occurred where the cell cannot immediately fire another signal

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propagation

the action potential propagates only in one direction, away from the origin of the nerve impulses, where the net result is nerve cells release neurotransmitters at their axon terminals or muscle cells contract

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action potential frequency

repeated ligand release by the stimulating nerve will cause repeated action potentials that can increase the strength of a cell’s response

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<p>neuromuscular junction (synapse)</p>

neuromuscular junction (synapse)

transfer site of a motor neuron action potential to skeletal muscle cell action potential

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three major parts of a synapse

presynaptic terminal with synaptic vesicles, synaptic cleft, postsynaptic membrane

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each muscle fiber is stimulated by a _____ of an axon

terminal branch

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<p>presynaptic (axon) terminal</p>

presynaptic (axon) terminal

contains the synaptic vesicles and acetylcholine

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<p>synaptic vesicles </p>

synaptic vesicles

membrane bound sacs that contain neurotransmitters

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<p>acetylcholine</p>

acetylcholine

the excitatory NT of the neuromuscular junction

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<p>acetylcholine receptors</p>

acetylcholine receptors

can only bind acetylcholine

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<p>synaptic cleft</p>

synaptic cleft

microscopic space that separates one neuron from the next cell in line

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<p>postsynaptic membrane</p>

postsynaptic membrane

the motor end plate of the synapse

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<p>beginning of NMJ…</p>

beginning of NMJ…

action potential propagates down the axon of the motor neuron and arrives at the presynaptic terminal

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<p>after the action potential arrives at the presynaptic terminal…</p>

after the action potential arrives at the presynaptic terminal…

depolarization causes voltage gated calcium channels to open and calcium diffuses inward

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<p>once calcium diffuses inward…</p>

once calcium diffuses inward…

the synaptic vesicles fuse with the axon membrane and release their neurotransmitter (ACh) into the synaptic cleft by exocytosis

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<p>after exocytosis of the neurotransmitter…</p>

after exocytosis of the neurotransmitter…

ACh diffuses across the cleft and binds onto its receptor (a ligand gated sodium channel) on the postsynaptic cell

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<p>after ACh binds onto it’s receptor…</p>

after ACh binds onto it’s receptor…

ligand gated sodium channels on the sarcolemma of the muscle fiber open and sodium diffuses inward causing a local depolarization

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<p>if enough local depolarizations are achieved to reach threshold…</p>

if enough local depolarizations are achieved to reach threshold…

an action potential is initiated in the skeletal muscle fiber

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<p>once an action potential is initiated…</p>

once an action potential is initiated…

neurotransmitter effects are then terminated after ACh is broken down to acetic acid and chlorine in the synaptic cleft

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spastic paralysis

continued stimulation of muscle fiber and eventual muscular fatigue, even death, caused by limited AChE activity

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flaccid paralysis

toxins that target ACh receptors and doesn’t allow ACh to bind so no muscle fiber stimulation

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myasthenia gravis

involves a shortage of ACh receptors that are thought to be caused by an autoimmune disorder

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symptoms of myasthenia gravis

drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness

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tetanus toxin

targets regulatory neurons that control release of ACh from presynaptic motor neurons and floods cleft with ACh and results in continued stimulation of muscle fiber and eventual muscular fatigue

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botulism toxin

blocks release of ACh from presynaptic cell and results in flaccid paralysis

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excitation-contraction coupling

sequence of events by which transmission of action potential along sarcolemma leads to sliding of actin and myosin myofilaments

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<p>beginning of excitation-contraction coupling sequence</p>

beginning of excitation-contraction coupling sequence

action potential that was initiated at the NMJ propagates along the sarcolemma until it reaches the T-tubules

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<p>once the action potential reaches the T-tubules…</p>

once the action potential reaches the T-tubules…

T-tubule invagination takes the sarcolemma depolarization into the sarcoplasmic reticulum

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<p>once at the sarcoplasmic reticulum…</p>

once at the sarcoplasmic reticulum…

depolarization in the T tubules causes voltage gated calcium channels to open and massive amounts of calcium diffuse into the sarcoplasm

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<p>while calcium is in the sarcoplasm…</p>

while calcium is in the sarcoplasm…

calcium binds to the regulatory protein troponin, changing its conformation and exposing the myosin binding site on actin for the first time

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<p>after the myosin binding site is exposed…</p>

after the myosin binding site is exposed…

myosin binds onto actin through cross bridge and contraction begins

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muscle fiber contraction

cross bridge activity

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what are the three steps of muscle fiber contraction?

cross bridge, power stroke, and recovery stroke

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cross bridge

myosin head binds actin and actin and myosin are now physically linked

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power stroke

myosin head pivots and bends, pulling the actin over the top of itself and the bare zone narrows

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recovery stroke

cocking of the myosin head where it is dislodged from the actin and returns to its prestroke high-energy position

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if calcium is still available because of continued stimulation during recovery stroke, then

the myosin head reengages

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after many quick repeats of muscle fiber contraction, what happens to the myosin heads and the sarcomere?

the myosin heads walk along the adjacent actin filaments and the sarcomere shortens and contraction is achieved in each fiber that has been stimulated by the neuron

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when does relaxation of a muscle fiber occur?

when no more active potential (stimulus) is present

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beginning of relaxation of muscle fiber

calcium ions are rapidly pumped back into the sarcoplasmic reticulum by active transport requiring ATP

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ATP is used to do what to myosin during relaxation

it dislodges the myosin from the actin and recocks the myosin heads

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what happens when free calcium is no longer present during relaxation?

troponin returns back to its original conformation and blocks the myosin binding sites on actin

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what is the final step of relaxation of the muscle fiber?

sarcomeres passively lengthen

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rigor mortis

actin and myosin in dying muscle cells become irreversibly cross linked after calcium and ATP synthesis ceases, so they gradually disappear as muscle proteins break down