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Final

PSL300H1 Study Guide - Final Guide: Depolarization, Motor Unit, Rise Time


Department
Physiology
Course Code
PSL300H1
Professor
Hae- Young Kee
Study Guide
Final

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NEUROMUSCULAR JUNCTION
Not like CNS synapse, more like family of synapses in parallel. Ach is the transmitter, sodium influx when Na+ binds to
Ach. The "end-plate" (at the muscle), always depolarizes the sarcolemma to threshold lvls (analogous to multiple
EPSPs spatial summation). Sarcolema has nicotine receptors.
Acetylcholinesterase: breaks down Ach, preventing it from hanging around. Secreted: from deep within the end-
plate, diffused to Ach (nicotinic) sites at the lip of the folds.
Poisoning the NMJ: BBB protects brain from toxins. Peripheral tissues exposed to toxins. 3 types of toxins to block
NMJ:
1. blocking Nicotinic AchR: curare, blocks nicotinic Ach receptor sites, preventing opening to cation channels in end
plate region, no AP generation in muscle fiber. (curare present -> blocks Ach receptors -> Ach doesn’t bind, sodium
channels can't open, prevents AP). Curariform drugs used as muscle relaxants.
2. block of exocytosis: botullinum toxin, prevents vesicle release from the terminals of the motor axon. End-plate
cannot be depolarized, no AP generated in muscle fiber. 
3. inhibition of Acetylcholinesterase: mechanism of organophosphate (nerve gases and pesticides). Ach won't be
broken down in NMJ, continuous depolarization at end-plate. Leads to paralysis by depolarization block, sodium
channels kept inactive.
TWITCHES, TETANUS AND TOXINS
The first action potential in the motor axon causes the muscle fiber to form a twitch contraction. Diff. rise times and
twitch forces, depends on muscle fiber type. Fast glycolytic -> fastest rise time, and the least duration time. fast
oxidative/glycotic, intermediate rise and duration time. slow oxidative -> slow rise time, longest duration. Isolated twitch
= useless. Force requires many twitches working together.
Tetanic contraction = summation of twitch force. In fast motor units, occurs if impulses discharge at 10/s or faster. 
impulses closely spaced in time, individual twitches fuse together into smooth rise of force, up to maximum sustainable
force for motor unit. When they fuse, they can contract a muscle group. Higher firing rates will increase rate of force,
but not give a higher sustained force.
Rate of discharge: maximum motor unit force attained by fused tetanus (30/s). Motor units fire at higher rates for brief
period of time, to increase contraction speed. But you're NOT increasing muscle force by contraction. Rate kept in
check by Renshaw cells.
Renshaw cells -> inhibitory cells, in ventral horn w/ motor neurons. Excited by axonal collaterals of motoneurons
before they leave the gray matter. Stop motoneurons from firing, form of control so motoneurons don't discharge too
long, too often or too actively. More activity of motoneurons = more renshaw cells activated.
Muscle AP: Ach binds and activates nicotinic receptor at endplate -> activation of nicotinic receptor opens NA+/K+
channel -> AP triggered. AP in muscles same as AP in axons, buut longer duration. AP travel from NMJ to both ends
of fiber, invading t-tubules.
T-tubules carry AP intro structures such as sarcoplasmic reticular, inside muscle fibers, activate Ach, activate Ca2+
release (Calcium from sarcoplasmic reticulum, not smooth muscle).

End-plate
Sarcolemma
acetylcholinestera
se
MUSCLES : STRIATED MUSCLES - MOTOR UNITS pt.2
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