Week 7 CH. 7 Excitation of a skeletal muscle

Question 1

Schwann cell (function and location)

Answer 1

insulate and speed signal
PNS

Question 2

Oligondendrocyte (function and location)

Answer 2

insulates and speeds signal in CNS

Question 3

saltatory conduction

Answer 3

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

Question 4

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

Answer 4

axon terminal, carry ACH. Release via exocytosis into synapse

Question 5

number of vesicles in terminal end plate

Answer 5

300,000

Question 6

Components of axon terminal (2)

Answer 6

1. mitochondira for ach synthesis
   2 vesicles (for ach trasnprot)

Question 7

Calcium channel in axon (role and how)

Answer 7

Calcium stimulates Ach secretion

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

Question 8

Role of protein kinase

Answer 8

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

Question 9

How does acetylcholine interact with muscle fibers?

Answer 9

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

Question 10

End plate potential

Answer 10

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

Question 11

How Ach in synaptic cleft cleared? (2)

Answer 11

1. diffusion
2. acetylcholinesterase

Question 12

Safety factor

Answer 12

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

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

Question 13

NMJ fatigue

Answer 13

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

Question 14

Curare

Answer 14

Ach inhibitor, does not allow EPP to reach threshold

Question 15

C-botulism toxin

Answer 15

Decreases amount of Ach released by nerve terminals

Question 16

After a few m.s Ach is

Answer 16

split by acetylcholinesterase into choline and acetate

Question 17

How is choline reabsorbed by neuron

Answer 17

Clathrin coated pits endocytose back into axon

Question 18

Methacholine mechanism

Answer 18

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

Question 19

Carbachol mechanism

Answer 19

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

Question 20

Nicotine mechanism

Answer 20

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

Question 21

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

Answer 21

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

i.e. laryngospasm

Methacholine, carbachol, nicotine

Question 22

Drugs that inactivate acetylcholineesterase

Answer 22

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

Question 23

What happens with drugs that inactive acetylcholinesterase?

Answer 23

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

can cause muscle spasm and death (laryngylspasm)

Question 24

Curariform drugs (MOA)

Answer 24

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

Question 25

Myasthenia gravis MOA

Answer 25

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

Question 26

Myasthenia gravis s/sx

Answer 26

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

Question 27

Myasthenia gravis treatment

Answer 27

neostigmine every few hours

Question 28

Transverse tubules

Answer 28

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

Question 29

Muscle action potential thresshold

Answer 29

-80 to -90

Question 30

Duration and speed of muscle action potential vs neuron action potential

Answer 30

Duration is longer and speed is slower

Question 31

How do T tubules work?

Answer 31

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

Question 32

Calcium release

Answer 32

from SR during AP

Question 33

Action potential of T-tubule causes

Answer 33

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

Question 34

Calcium release:

Answer 34

releases into sarcoplasm, surrounds myofibrils and causes contraction

Question 35

How is calcium removed after contraction?

Answer 35

Pumped with ATP back into sarcoplasmic tubles via calcium pump

Question 36

Calquesterin

Answer 36

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

Question 37

Rigor mortis occurs

Answer 37

3-4 hours after death

Question 38

What causes rigor mortis (2 reasons)?

Answer 38

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.

Question 39

excitatory pulse of calcium ions

Answer 39

1/20 seconds long amount of calcium is 500x increased

Question 40

Protein Kinase

Answer 40

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

Question 41

Synapsin

Answer 41

frees Ach into active zone for exocytosis