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Muscle contraction summary

1. Generation of nerve impulse
2. Impulse transmission and muscle cell depolarization
3. Release of Ca⁺⁺ from SR into cytoplasm
4. Exposure of myosin binding sites
5. Binding of myosin to actin → "Power Stroke"

Motor unit

Consists of a motor axon and all of the muscle cells it contacts; number of cells in unit varies throughout body and determines precision of muscle movement

Motor endplate

specialized contact created by the fanned out membranes of a motor axon at the myoneuronal junction

Primary synaptic cleft

shallow invagination of the sarcolemma closely apposed (touching, more or less) the motor endplate

Secondary synaptic clefts

smaller infoldings of the sarcolemma that increase the total surface area of the nerve/muscle contact

Synaptic transmission/depolarization

Release of acetylcholine into synaptic cleft from vesicles in the motor axon terminal results in:
1. activation of ach. receptors on sarcolemma
2. opening of ligand-gated Na⁺ channels in sarcolemma (initial depolarization)
3. opening of voltage-gated Na⁺ channels in sarcolemma (widespread muscle cell depolarization)

Release of Ca⁺⁺ from SR (initial theory)

Depolarization of sarcolemma stimulates inositol triphosphate (IP₃) formation, which then binds to an IP₃-sensitive Ca⁺⁺ channel in the terminal cisternae of the SR membrane. Ca⁺⁺ is released through these channels causing ↑ intracellular Ca⁺⁺.

Release of Ca⁺⁺ from SR (current theory)

Depolarization of sarcolemma activates a dihydropyridine (DHPD) receptor in the sarcolemma which is mechanically coupled to ryandine receptors (Ca⁺⁺ channels) on the inner leaflet. Ca⁺⁺ is released through these channels causing ↑ intracellular Ca⁺⁺.

Exposure of myosin binding sites

Intracellular Ca⁺⁺ binds to Tnc subunit of the troponin complex on actin, resulting in a lateral rotation of tropomyosin strand, driving it deeper into groove btw. actin helices and exposing myosin binding sites

Binding of myosin to actin

"Power stroke"; myosin extends out and binds to actin releasing Pi from myosin head → allows the release of ADP from myosin head causing myosin neck to flex or "snap". Flexion of many myosin heads ratchets the actin filament along the myosin thus shortening the sarcomere.

Rigor complex

Configuration following power stroke where myosin remains attached to actin filament until ATP binds to myosin head; ATP is then hydrolyzed to ADP and Pi to restart the process

Muscle relaxation summary

1. Ca⁺⁺ transported back into lateral cisternae of SR
2. Detachment of Ca⁺⁺ from Tnc subunit → tropomyosin shifts out of groove and myosin binding sites are recovered

Calcium removal (during muscle relaxation)

Ca⁺⁺/ATPase ion pump on lateral cisternae of SR actively transports Ca⁺⁺ back into SR lumen where it will bind to calsequestrin restoring intracellular Ca⁺⁺ levels

Major uses for ATP in muscles

1. Powers the myosin-actin "power stroke" by allowing the hydrolysis of ATP to ADP and Pi (50%)
2. Required to break rigor complex (doesn't "use up" ATP, creatine kinase produces it)
3. Powers Ca⁺⁺/ATPase ion pump on SR (50%)
* req. muscle tissue to be well adapted to rapidly generate APT

Afferent nerve endings in muscles

Carry info toward CNS from the muscle
1. muscle spindles (stretching)
2. tendon organs (tension)
3. Joint receptors (joint position)

Muscle spindles

length registering receptors; fusiform structure, short, variable in number (most numerous in fine control muscles), longitudinal orientation, composed of intrafusal fibers enclosed in a CT capsule

Intrafusal fibers

Specialized muscle fibers of the muscle spindle that have fewer myofibrils and are not designed for contraction; Types: nuclear bag fibers and nuclear chain fibers

Annulospiral (primary) endings

large sensory fibers spiraled around intrafusal fibers of muscle spindles

Flower spray (secondary) endings

small sensory fibers terminating in spray-like arbor on nuclear chain fibers of muscle spindles

Function of intrafusal fiber afferent endings

respond to muscle stretch by creating neural impulse, provides CNS with info about the state of contraction of a given muscle

Muscular Dystrophy

genetic disorder characterized by chronic progressive muscle loss; X-link recessive mutation in gene coding for dystrophin → loss results in destabilization of cell membrane which ruptures during repeated contraction → profound muscle loss → death from cumulative damage to cardiac and respiratory muscle cells.

Myasthenia Gravis

autoimmune disorder characterized by chronic progressive muscle weakness. Antibodies block Ach receptors at the neuromuscular junction → decline in total number of receptors→ reduction in the muscle excitation/contraction. Can be treated with ACh esterase (AChE) blockers.

Efferent somatic motor neurons

Carries info from CNS to muscle; located in the ventral horn of the spinal cord; initial signal for muscle contraction arises from nerve impulses generated by these then transferred along their myelinated axons and terminating at the neuromuscular/myoneuronal junction


contained in numberous intracellular vesicles in terminal ends of motor axons; sarcolemma membrane adjacent to synaptic cleft contains specialized receptors for it; its binding initiates depolarization

Action potential of skeletal muscle

1. Na⁺ influx (depolarization)
2. K⁺ efflux (repolarization)

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