| Term | Definition |
|---|
| ca2+ | internal regulator of contraction |
| somatic nervous system | controls muscle fibers. will control availability of ca2+. |
| somatic motor neuron | one somatic motor neuron can control many muscle fibers. each skeletal muscle fiber is controlled by one somatic motor neuron. axon terminals contain vesicles of acetylcholine ach |
| motor unit | one somatic motor neuron and all the skeletal muscle fibers it controls. (all muscle fibers f motor unit contract together) |
| neuromuscular junction | site of interaction between somatic motor neuron and muscle fiber |
| acetylcholine | is a neurotransmitter |
| motor end plate | region of sarcolemma opposite of the synaptic end bulbs. it has ACH receptors. has voltage gated na+ and k+ channels. ligand na+ channels. |
| ACH receptors | bind ACH, opens na+ channel influx of na+. depolarization |
| acetylcholinesterase (ache) | enzyme that breaks down ach from synaptic cleft and ach receptors. products are recycled by to axon terminal. shuts na+ channels on ach receptors. therefore, no more action potentials on sarcolemma |
| calsequestrin | ca2+ transport protein in terminal cisterns that pumps ca2+ back into terminal cisterns |
| 1st step | action potential on axon terminal causes release of ach into the synaptic cleft |
| 2nd step | ACH diffuses across the synaptic cleft and binds to ACH receptors. this causes a change in the conformation of the receptor and opens the channel na+ influx causes depolarization of the motor end plate. |
| 3rd step | if enough ach is released to open enough ach receptors and the na+ influx causes a depolarization to treshold. and action potential occurs on the moto end plate and then propagates across the entire sarcolemma. |
| 4th step | the ap on the sarcolemma travels into the t tubules and causes ca2+ to be released from the terminal cisterns. ca2+ diffuses through the cell and binds to troponin. this causes the event of the sliding filament theory. |
| 5th step | to end the contraction, aps stop on the axon terminal and no more ach is released. ache in the synaptic cleft removes ach and shuts the na+ channels on ach receptors, therefore, no more ap on sarcolemma. calsequestrin pump ca2+ back into terminal cisterns using atp. muscle fiber relaxes. |
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