Lecture 5 - Neuromuscular Junction Flashcards Preview

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Flashcards in Lecture 5 - Neuromuscular Junction Deck (25):
1

What is the direct result of the arrival of an action potential at the telodendria?

Opening of voltage gated calcium channels.

2

Describe the importance of voltage-gated calcium channels in the pre-synaptic neuron.

These voltage gated Ca2+ channels allow the influx of Ca2+ into the neuron. When this occurs, synaptic vesicles fuse with the P.M., and release NT into the synaptic cleft.

3

What is found in abundance in the telodendria?

Mitochondria (used to generate ATP for Na/K pump activity)

4

Describe (overall) how action potentials are transmitted between cells.

The action potential is transmitted from neuron to muscle via the neuromuscular junction.

5

A? 

Purpose?

Q image thumb

Mitochondria

Reset the membrane potential for the propagation of the next action potential.

6

B?

Function?

Q image thumb

Short filament

Binds the NT vesicle to the dense bar prior to NT release; "tether"

7

C?

Function?

Q image thumb

Dense bar

Unkown function; thought to help "anchor" the NT vesicle prior to NT release

8

D?

Function?

Q image thumb

Subneural cleft

Acts to increase the surface area for neuron/end plate/receptor interaction.

9

E?

Function?

Q image thumb

Acetylcholinesterase

Degrades ACh in the neural cleft; prevents tetany

10

F?

Function?

Q image thumb

ACh-R

Receives NT to produce depolarization of end plate

11

Acetylcholine receptors have __ alpha subunits, and require binding of two ACh molecules to open.

2

12

Responsible for production of the local potential on the motor end plate.

2 ACh molecules binding to the ACh-R; produces an opening to the lingand-gated ACh-R; this opens the channels and allows Na+ to enter the muscle at the sarcolemma

13

Ways by which ACh is removed from the synaptic cleft

Re-uptake (using ATP driven pumps)

Diffusion (random and slow)

Destruction by acetylcholinesterase

14

ACh is produced in the _____.

liver

15

How does ACh binding cause transmission of the action potential?

1) Two ACh molecules bind to the ACh-R

2) Binding causes the opening of sodium channels, which causes a LOCAL potential

3) If the local potential is large enough, voltage-gated Na+ channels are opened, and THESE produce the "end plate potential" that moves down the sarcolemma

16

What is the voltage of the "end plate potential"?

50-75 mV

17

These are formed at the plasma membrane to form new vesicles for ACh received from the liver.

Clathrin coated pits (become vesicles)

18

Methacholine binds to ACh-R and acts to ____.

produce depolarization of the motor-end plate

19

Carbachol acts to ____ and produce depolarization of the motor-end plate

bind to ACh-R

20

Nicotine binds to ACh-R and produces _____

end plate depolarization

21

How do methacholine, carbachol, and nicotine continue to bind to ACh-R and produce potentials?

By being non-susceptible to breakdown by ACh-Esterase 

22

What drug inhibit AP transmission?

Competitievly binds to ACh-R, preventing depolarization through ACh binding

23

What drugs prevent functioning of acetylcholinesterase?

Neostygmine, physostygmine, diisopropyl flurophosphates

24

Explain the pathophysiology of myasthenia gravis.

Auto-aby are formed against ACh-R; as a result, there is muscle weakness due to destruction of -R and no action potentials. 

25

Explain the treatment of myasthenia gravis

Because of auto-aby mediated destruction of ACh-R, neostigmine is used to inhibit acetylcholinesterase. This ACh-E inhibition allows enough free ACh to remain in the synaptic cleft to (hopefully) bind to any free ACh-R and trigger an action potential.