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"
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
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
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.
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)
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
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
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.
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