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Physiology > Week 7 CH. 7 Excitation of a skeletal muscle > Flashcards

Week 7 CH. 7 Excitation of a skeletal muscle Flashcards

1
Q

Schwann cell (function and location)

A

insulate and speed signal
PNS

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2
Q

Oligondendrocyte (function and location)

A

insulates and speeds signal in CNS

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3
Q

saltatory conduction

A

“hopping” down axon, speeds up signal. Schwann and oligondendrocytes allow

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4
Q

synaptic vesicles in motor nueron - role and how they work.

A

axon terminal, carry ACH. Release via exocytosis into synapse

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5
Q

number of vesicles in terminal end plate

A

300,000

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6
Q

Components of axon terminal (2)

A
  1. mitochondira for ach synthesis
    2 vesicles (for ach trasnprot)
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7
Q

Calcium channel in axon (role and how)

A

Calcium stimulates Ach secretion

Voltage gated calcium channels open, allowing calcium to diffuse into axon, activate protein kinase

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8
Q

Role of protein kinase

A

phosphorylates synapsin, signaling Ach vesicles to move to active zone and endocytose

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9
Q

How does acetylcholine interact with muscle fibers?

A

Via acetylcholine-gated ion channels on sarcolemma - channels open when 2 Ach bind and allows Na+ to flow in.

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10
Q

End plate potential

A

Flow of Na+ ions into muscle fiber causes action potential in muscle for contraction

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11
Q

How Ach in synaptic cleft cleared? (2)

A
  1. diffusion
  2. acetylcholinesterase
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12
Q

Safety factor

A

Normal impulse is 3X what is required for EPP to stimulate muscle

i.e. ACH released is 3x than what is necessary

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13
Q

NMJ fatigue

A

stimulation greater than 100 times/second for several minutes lowers Ach vesicles, so too few pass into muscle fiber

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14
Q

Curare

A

Ach inhibitor, does not allow EPP to reach threshold

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15
Q

C-botulism toxin

A

Decreases amount of Ach released by nerve terminals

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16
Q

After a few m.s Ach is

A

split by acetylcholinesterase into choline and acetate

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17
Q

How is choline reabsorbed by neuron

A

Clathrin coated pits endocytose back into axon

18
Q

Methacholine mechanism

A

Causes cation channels to open because it is very similar to Ach

19
Q

Carbachol mechanism

A

Causes cation channels to open because it is very similar to Ach

20
Q

Nicotine mechanism

A

Causes cation channels to open because it is very similar to Ach

21
Q

Drugs that are similar to Ach - why do they persist?

A

acetylcholinesterase does not target them, so we have a localized state of muscle spasm

i.e. laryngospasm

Methacholine, carbachol, nicotine

22
Q

Drugs that inactivate acetylcholineesterase

A
  1. neostigmine
  2. physostigmine
  3. diisopropyl fluorophosphate (nerve gas)
23
Q

What happens with drugs that inactive acetylcholinesterase?

A

Ach accumulates because Ach-esterase cannot cleave ACH and there is continuous muscle fiber stimulation

can cause muscle spasm and death (laryngylspasm)

24
Q

Curariform drugs (MOA)

A

d-tubocurarine blocks passage of nerve impulses from nerve ending to muscle by blocking actin of Ach on receptor

25
Q

Myasthenia gravis MOA

A

Shortage of Ach recepotrs because person’s ACh receptors are attacked by own antibodies

26
Q

Myasthenia gravis s/sx

A

drooping upper eyelids, difficulty swallowing and talking, generalized muscle weakness

27
Q

Myasthenia gravis treatment

A

neostigmine every few hours

28
Q

Transverse tubules

A

Penetrate deep into muscle fiber so that current flow of AP can reach deep within the fiber

29
Q

Muscle action potential thresshold

A

-80 to -90

30
Q

Duration and speed of muscle action potential vs neuron action potential

A

Duration is longer and speed is slower

31
Q

How do T tubules work?

A

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

32
Q

Calcium release

A

from SR during AP

33
Q

Action potential of T-tubule causes

A

current flow into SR csiternae next to T tubule, triggering calcium release

34
Q

Calcium release:

A

releases into sarcoplasm, surrounds myofibrils and causes contraction

35
Q

How is calcium removed after contraction?

A

Pumped with ATP back into sarcoplasmic tubles via calcium pump

36
Q

Calquesterin

A

calcium binding protein in SR (holds onto calcium so that it cannot all diffuse out of SR)

37
Q

Rigor mortis occurs

A

3-4 hours after death

38
Q

What causes rigor mortis (2 reasons)?

A

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.

39
Q

excitatory pulse of calcium ions

A

1/20 seconds long

amount of calcium is 500x increased

40
Q

Protein Kinase

A

Activated by calcium
phosphorylates synapsin—>frees Ach into active zone

41
Q

Synapsin

A

frees Ach into active zone for exocytosis

Physiology (13 decks)

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