PSL300H1 Study Guide - Final Guide: Depolarization, Motor Unit, Rise Time
ProfessorHae- Young Kee
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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
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).
MUSCLES : STRIATED MUSCLES - MOTOR UNITS pt.2
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