Chapter 6- Excitation in Skeletal and Motor Units

somatic motor neurons

motor neurons that activate muscle fibers & reside in spinal cord. each has an axon that extends from the cell body in the spinal cord to the muscle fiber

axons attached to neurons

branch as it enters the muscle so it can innervate multiple muscle fibers. each muscle fiber also only has one NMJ

motor end plate

the region of the muscle fiber plasma membrane that lies directly under the terminal portion of the axon

neuromuscular junction (NMJ)

junction of an axon terminal with the motor end plate, synapse between a somatic motor neuron and a skeletal muscle fiber

neural part of NMJ

axon terminal and synaptic end bulbs which contain synaptic vesicles with Ach (Acetylcholine)

muscular part of NMJ

motor plate, acetyl choline receptors

synapse

region of communication between 2 neurons/neuron-target cell (has synaptic cleft and neurotransmitter)

synaptic cleft

the end of the axon and the muscle fiber separated (50-80 nm)

synaptic vesicles

within axon terminals and also contain neurotransmitter (Acetylcholine)

junctional folds

at the NMJ, the muscle fiber sarcolemma is highly folded and known as this. they provide a large surface for locating acetylcholine receptors

a nerve impulse elicits muscle action potential

ACh release, activation of ACh receptors, production of muscle action potential, termination of ACh activtity

acetylcholine-gated ion channels

two ACh molecules attach to the alpha subunit which causes a conformational change that opens the channel

end plate potential

sodium ion flow inside the muscle fiber creates local positive potential

acetylcholinesterase

ACh is destroyed by this

synaptic space

small amount of ACh diffuses out

when end plate potential is generated at neuromuscular junction

causes a wave of depolarization that spreads to adjacent sarcolemma

depolarization

generating and propagating an action potential

depolarization of sarcolemma

opens voltage-gated sodium channels, allowing Na+ to enter. AP is generated and spreads and propagates along sarcolemma in all directions

repolarization

restores the sarcolemma to its initial polarized state (negative inside and positive outside)

repolarization sarcolemma

consequence of opening and closing ion channels, Na+ close and K+ opens. potassium is higher in cell than extracellular fluid so it diffuses out of muscle fiber and restores sarcolemma to rest

releasing ACh steps

AP arrives at axon terminal of motor neuron, voltage-gated Ca+2 channels enter axon terminal, moving down gradient, Ca+2 causes ACh release by exocytosis

ACh binding

opens gated ion channel that allows passage of Na+ into muscle fiber and K+ out. leads to change in membrane potential. ACh is then brokendown in synaptic cleft by AChe

botulism

toxin blocks exocytosis of synaptic vesicles at neuromuscular junction, ACh is not released and skeletal muscles become paralyzed

excitation-contraction coupling

sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments (muscle contraction)

increased levels of cytosolic Ca+2

activates contractile appartus, produced by electrical activity from E-C coupling

current of Action potential

required for contraction to penetrate deeply into muscle fibers

T tubules

action potential travels along this and penetrates all the way through muscle fiber, known as internal extensions of cell membrane

T Tubule AP

causes release of Ca+2 inside the muscle fiber

traits of T-tubules

open to exterior of muscle fiber, penetrate from one side of muscle fiber to opposite fiber and communicate with extracellular fluid

dihydropyridine (DHP) receptor

located in T-tubule. is voltage gated Ca+2 channel, responsible for inducing a conformational change to open ryanodine receptor channels

Ryanodine receptor

located in SR membrane, connects to the DHP receptor and forms Ca+2 release channel.

terminal cisternae of SR

Ca+2 is released from here and is sent to cytosol where it binds to troponin

Increase in Ca2+

starts muscle contraction

muscle resting state

low Ca2+ in cytosol, troponin-tropomyosin complex keeps the actin filaments inhibited and maintains muscles in state

muscle excitation state

Ca+2 concentration increases, calcium pulse lasts 1/20 of a second

contraction ends

removal of Ca+2 from troponin

Ca+2-ATP-ases pump

pumps Ca+2 from the cytosol back to SR, causing Ca2+ levels in sarcoplasm to decrease

inside the SR

calsequestrin protein is released which binds calcium

steps in E-C coupling

(1)action potential propagates along sarcolemma and down T tubule, calcium ions are released

(2) tubules change shape ad open Ca2+ release channels in terminal cisterns of sarcoplasmic reticulum

(3) calcium binds to troponin and removes the blocking action of tropomyosin, myosin binding sites on thin filaments are exposed

(4) contraction begins and myosin binding to actin forms bridges and contraction.

sequence of events for contraction

motor neuron fires AP down axon

terminal releases AcH into synaptic cleft

ACh receptors on junctional folds of sarcolemma

ACh causes EPP, triggers an AP in sarcolemma

AP travels down t tubules

Ca2+ released from sarcoplasmic reticulum

Ca2+ binds to troponin and myosin heads bind to actin

contraction occurs

motoneurons that leave spinal cord

innervates multiple muscle fibers

motor unit

consists of a somatic motoneuron plus all of the skeletal muscle fibers it stimulates. all muscle fibers in this contract in unison.

muscle twitch

a single stimulus-contraction-relaxation sequence in a muscle fiber

three phases of a twitch

latent, contraction, relaxation

latent period

lasts 2 msec, AP travels across sarcolemma, SR releases CA+2, muscle fiber does not produce tension

contraction phase

lasts 15msec, tension rises & Ca2+ bind to troponin, cross-bridges interactions are occurring

relaxation phase

lasts 25 msec, Ca+2 levels are falling, myosin binding sites are covered by tropomyosin, cross-bridges detached, and tension falls to resting levels

refractory period

period in which the muscle fiber loses its excitability and cannot respond to a second stimuli

manual twitch

when the muscle is stimulated with a single electric shock, it contracts and relaxes

summation

if a second electric shock is delivered immediately after, it will produce a second twitch increasing the response

incomplete tetanus

if stimulation is delivered an increasing frequency, the relaxation time between successive twitches gets shorter

complete tetanus

when no relaxation takes place between twitches, contraction is sustained

spinal muscular atrophy

genetic disorder characterized by weakness and atrophy of skeletal muscle due to the loss of motor neurons