Nerve Stimulus Excites the Muscle Cell A muscle

Nerve Stimulus Excites the Muscle Cell • A muscle cell must receive a stimulus to begin the excitation-contraction coupling – Series of events linking electrical signal to muscle contraction – Muscle cells can be stimulated by ACh • ACh- Acetylcholine- neurotransmitter 1. Nerve impulse reaches axon terminal • Axon- long extension of nerve cell, relays stimulus • Neuromuscular Junction- axon branches as it enters muscle, each branch goes to 1 muscle fiber • Synaptic cleft- small space between axon terminal & muscle fiber 2. Voltage-gated Ca 2+ channels on axon terminal open Ca 2+ goes in synaptic vesicles fuse with membrane • Synaptic vesicles- sacs filled with neurotransmitter 3. Exocytosis of ACh • Motor end plate- folded part of sacrolemma with millions of ACh receptors Animated Neurotransmission

Resting Potential- Polarized • Partial negative charge inside a neuron or muscle cell at rest – More K+ inside, more Na+ outside – Both K+ & Na+ diffuse through cell membrane, K+ can get out easier than Na+ can get in – Polarized- difference in charge inside & outside the cell Resting membrane potential K+ - K+ K+ Na+ - Na+ K+ Na+ K K+ K+ - ++ Na K Outside the cell Membrane Na+ Na K+ + Cytoplasm + K+ Na+ K+ - Na+ K+ + K K+ K+ -

Action Potential (AP)- Depolarized • When muscle cell is stimulated by ACh, chemically gated ion (Na+ & K+) channels open • Na+ flows in faster than K+ flows out Depolarization- change of charge (action potential) – Causes a ripple effect along sarcolemma, voltage gated Na+ gates open – Also causes slower K+ gate to open, K+ rushes out Repolarization- return to resting charge • Active transport is used to move Na+ back outside & K+ back inside – Refactory period- cell cannot be stimulated again until repolarization & active transport of ions is complete Animated Neurotransmission K+ - K+ K+ Na+ Na+ - + Na Na+ K+ ++ + Na K K + Na + Outside the cell K K+ - Na+ Membrane K+ Na+ K+ ++ Na K + K - + Cytoplasm + + K Na Na Na+ K+ Na+ K + Action Potential

Excitation-Contraction Coupling • AP ends before signs of contraction are obvious 1. AP goes along sacrolemma & down T tubules • AP in T tubules causes release of Ca 2+ from adjacent terminal cisternae 2. Ca 2+ binds to troponin, causing it to move myotroponin away for actin active site 3. Mysosin heads form cross bridges with active sites on actin & pull thin filaments toward center of sacromere (power stroke) Excitation-Contraction Coupling 2 Actin Myosin Bridge

ATP and the Power Stroke • Myosin heads have ATP attached to them, used for E to “cock” heads back – Release ADP & P • Myosin attaches to active sites to form “cross-bridges” • Myosin head returns to its lower E position once cross bridge is formed, moving the thin filament (power stroke) • ATP binds to myosin head, actin filament is released Actin Myosin Bridge

Contraction • Full contraction of the muscle cell requires 30+ repeats of power stroke action – Process repeats until Ca 2+ is no longer available • Acetylcholinesterase – enzyme that digests acetylcholine to ensure contraction does not persist without nervous stimulation • No more acetylcholine Ca 2+ is reabsorbed by SR by active transport (uses more ATP) Actin Myosin Bridge

Rigor Mortis • When breathing stops, no more O 2 can’t make ATP • Dying cells cannot keep extracellular Ca 2+ out – Ca 2+ goes into muscle cells and promotes myosinactin cross-bridges – ATP is still being consumed at the cross bridge, when it runs out, detachment becomes impossible stiffness • Usually starts to set in 3 -4 hrs postmortem, peaks about 12 hrs postmortem – As muscle protein begin to break down, rigor mortis gradually goes away