Week 7 CH. 7 Excitation of a skeletal muscle Flashcards
Schwann cell (function and location)
insulate and speed signal
PNS
Oligondendrocyte (function and location)
insulates and speeds signal in CNS
saltatory conduction
“hopping” down axon, speeds up signal. Schwann and oligondendrocytes allow
synaptic vesicles in motor nueron - role and how they work.
axon terminal, carry ACH. Release via exocytosis into synapse
number of vesicles in terminal end plate
300,000
Components of axon terminal (2)
- mitochondira for ach synthesis
2 vesicles (for ach trasnprot)
Calcium channel in axon (role and how)
Calcium stimulates Ach secretion
Voltage gated calcium channels open, allowing calcium to diffuse into axon, activate protein kinase
Role of protein kinase
phosphorylates synapsin, signaling Ach vesicles to move to active zone and endocytose
How does acetylcholine interact with muscle fibers?
Via acetylcholine-gated ion channels on sarcolemma - channels open when 2 Ach bind and allows Na+ to flow in.
End plate potential
Flow of Na+ ions into muscle fiber causes action potential in muscle for contraction
How Ach in synaptic cleft cleared? (2)
- diffusion
- acetylcholinesterase
Safety factor
Normal impulse is 3X what is required for EPP to stimulate muscle
i.e. ACH released is 3x than what is necessary
NMJ fatigue
stimulation greater than 100 times/second for several minutes lowers Ach vesicles, so too few pass into muscle fiber
Curare
Ach inhibitor, does not allow EPP to reach threshold
C-botulism toxin
Decreases amount of Ach released by nerve terminals
After a few m.s Ach is
split by acetylcholinesterase into choline and acetate
How is choline reabsorbed by neuron
Clathrin coated pits endocytose back into axon
Methacholine mechanism
Causes cation channels to open because it is very similar to Ach
Carbachol mechanism
Causes cation channels to open because it is very similar to Ach
Nicotine mechanism
Causes cation channels to open because it is very similar to Ach
Drugs that are similar to Ach - why do they persist?
acetylcholinesterase does not target them, so we have a localized state of muscle spasm
i.e. laryngospasm
Methacholine, carbachol, nicotine
Drugs that inactivate acetylcholineesterase
- neostigmine
- physostigmine
- diisopropyl fluorophosphate (nerve gas)
What happens with drugs that inactive acetylcholinesterase?
Ach accumulates because Ach-esterase cannot cleave ACH and there is continuous muscle fiber stimulation
can cause muscle spasm and death (laryngylspasm)
Curariform drugs (MOA)
d-tubocurarine blocks passage of nerve impulses from nerve ending to muscle by blocking actin of Ach on receptor
Myasthenia gravis MOA
Shortage of Ach recepotrs because person’s ACh receptors are attacked by own antibodies
Myasthenia gravis s/sx
drooping upper eyelids, difficulty swallowing and talking, generalized muscle weakness
Myasthenia gravis treatment
neostigmine every few hours
Transverse tubules
Penetrate deep into muscle fiber so that current flow of AP can reach deep within the fiber
Muscle action potential thresshold
-80 to -90
Duration and speed of muscle action potential vs neuron action potential
Duration is longer and speed is slower
How do T tubules work?
Contain extracellular fluid, act as internal extensions of the sarcolemma.
Surrounded by electrical current so that they can eliect muscle contraction
potential charge spreads along the tubule
Calcium release
from SR during AP
Action potential of T-tubule causes
current flow into SR csiternae next to T tubule, triggering calcium release
Calcium release:
releases into sarcoplasm, surrounds myofibrils and causes contraction
How is calcium removed after contraction?
Pumped with ATP back into sarcoplasmic tubles via calcium pump
Calquesterin
calcium binding protein in SR (holds onto calcium so that it cannot all diffuse out of SR)
Rigor mortis occurs
3-4 hours after death
What causes rigor mortis (2 reasons)?
Intracellular calcium levels increase because ATP is no longer being synthesized, so calcium cannot be pumped. back into SR
No ATP for cross bridge detachment, so muscles stay contracted.
excitatory pulse of calcium ions
1/20 seconds long
amount of calcium is 500x increased
Protein Kinase
Activated by calcium
phosphorylates synapsin—>frees Ach into active zone
Synapsin
frees Ach into active zone for exocytosis
