Lecture 5 - Neuromuscular Junction

Question 1

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

Answer 1

Opening of voltage gated calcium channels.

Question 2

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

Answer 2

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.

Question 3

What is found in abundance in the telodendria?

Answer 3

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

Question 4

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

Answer 4

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

Question 5

A?

Purpose?

Answer 5

Mitochondria

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

Question 6

B?

Function?

Answer 6

Short filament

Binds the NT vesicle to the dense bar prior to NT release; “tether”

Question 7

C?

Function?

Answer 7

Dense bar

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

Question 8

D?

Function?

Answer 8

Subneural cleft

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

Question 9

E?

Function?

Answer 9

Acetylcholinesterase

Degrades ACh in the neural cleft; prevents tetany

Question 10

F?

Function?

Answer 10

ACh-R

Receives NT to produce depolarization of end plate

Question 11

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

Answer 11

2

Question 12

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

Answer 12

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

Question 13

Ways by which ACh is removed from the synaptic cleft

Answer 13

Re-uptake (using ATP driven pumps)

Diffusion (random and slow)

Destruction by acetylcholinesterase

Question 14

ACh is produced in the _____.

Answer 14

liver

Question 15

How does ACh binding cause transmission of the action potential?

Answer 15

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

Question 16

What is the voltage of the “end plate potential”?

Answer 16

50-75 mV

Question 17

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

Answer 17

Clathrin coated pits (become vesicles)

Question 18

Methacholine binds to ACh-R and acts to ____.

Answer 18

produce depolarization of the motor-end plate

Question 19

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

Answer 19

bind to ACh-R

Question 20

Nicotine binds to ACh-R and produces _____

Answer 20

end plate depolarization

Question 21

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

Answer 21

By being non-susceptible to breakdown by ACh-Esterase

Question 22

What drug inhibit AP transmission?

Answer 22

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

Question 23

What drugs prevent functioning of acetylcholinesterase?

Answer 23

Neostygmine, physostygmine, diisopropyl flurophosphates

Question 24

Explain the pathophysiology of myasthenia gravis.

Answer 24

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

Question 25

Explain the treatment of myasthenia gravis

Answer 25

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.