Nerve Stimulus Excites the Muscle Cell A muscle cell must receive a stimulus to begin the excitation-contraction couplingA 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- neurotransmitterACh- Acetylcholine- neurotransmitter 1.Nerve impulse reaches axon terminal Axon- long extension of nerve cell, relays stimulusAxon- long extension of nerve cell, relays stimulus Neuromuscular Junction- axon branches as it enters muscle, each branch goes to 1 muscle fiberNeuromuscular Junction- axon branches as it enters muscle, each branch goes to 1 muscle fiber Synaptic cleft- small space between axon terminal & muscle fiberSynaptic 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 neurotransmitterSynaptic vesicles- sacs filled with neurotransmitter 3. Exocytosis of ACh Motor end plate- folded part of sacrolemma with millions of ACh receptorsMotor 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 restPartial 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 Membrane Outside the cell Cytoplasm Na + K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ - K+K+ K+K+ K+K+ K+K Resting membrane potential

Action Potential (AP)- Depolarized When muscle cell is stimulated by ACh, chemically gated ion (Na + & K + ) channels openWhen 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)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 insideActive 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 Membrane Outside the cell Cytoplasm Na + K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ - K+K+ K+K+ K+K+ K+K+ Action Potential Potential Na + Animated Neurotransmission

Excitation-Contraction Coupling AP ends before signs of contraction are obviousAP 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 cisternaeAP 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) Actin Myosin Bridge Excitation-Contraction Coupling Excitation-Contraction Coupling 2

ATP and the Power Stroke Myosin heads have ATP attached to them, used for E to “cock” heads backMyosin 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 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)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 releasedATP binds to myosin head, actin filament is released Actin Myosin Bridge

Contraction Full contraction of the muscle cell requires 30+ repeats of power stroke actionFull contraction of the muscle cell requires 30+ repeats of power stroke action –Process repeats until Ca 2+ is no longer available AcetylcholinesteraseAcetylcholinesterase –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)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 ATPWhen breathing stops, no more O 2  can’t make ATP Dying cells cannot keep extracellular Ca 2+ outDying cells cannot keep extracellular Ca 2+ out –Ca 2+ goes into muscle cells and promotes myosin- actin cross-bridges –ATP is still being consumed at the cross bridge, when it runs out, detachment becomes impossible  stiffness Usually starts to set in 3-4hrs postmortem, peaks about 12 hrs postmortemUsually starts to set in 3-4hrs postmortem, peaks about 12 hrs postmortem –As muscle protein begin to break down, rigor mortis gradually goes away