Action Potential Propagation and End Plate Potentials Flashcards Preview

Physiology Unit 1 > Action Potential Propagation and End Plate Potentials > Flashcards

Flashcards in Action Potential Propagation and End Plate Potentials Deck (10)
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1
Q

What is the length constant? How does this influence AP propagation?

A

Term describing how far depolarization spreads as a function of axon diameter.

It is the length by which it takes the depolarization signal to fall by 1/e (~37%). If length constant is larger, you can start Hodgkin cycle at a more distant patch of membrane, increasing conduction speed.

2
Q

What two factors increase the conduction velocity?

A
  1. Larger diameter of axon

2. Myelination of axon which is interrupted at nodes of Ranvier

3
Q

What are the two effects of myelination?

A
  1. Resistance of membrane increases -> less current can leak out of the myelinated section, allowing a depolarizing signal to travel farther
  2. Capacitance is decreased, so less charge can be held and threshold potential is reached FASTER
4
Q

What structures are on the presynaptic membrane at the neuromuscular junction?

A
  1. Voltage-dependent calcium channels

2. Synaptic vesicles containing the neurotransmitted Acetylcholine

5
Q

How large in the synaptic cleft?

A

Larger than a neuronal synapse, about 50-100mm

6
Q

What does the post-synaptic membrane contain at the neuromuscular junction?

A
  1. Acetylcholine receptors

2. Acetylcholinesterase

7
Q

How is acetylcholine released into the synaptic cleft?

A

Voltage dependent Ca+2 channels open. Calcium triggers vesicles to fuse with the presynaptic membrane at fusion pores.

8
Q

What is the synaptic delay? What causes this?

A

Delay between presynaptic action potential and post-synaptic action potential being relayed.

Caused by mechanisms of vesicle release taking time, normally about 0.5-1 msec

9
Q

What nicotinic acetylcholine receptors? How do they differ from muscarinic?

A

They are ligand-gated ion channels, they bind acetylcholine or nicotine as an agonist to allow both sodium and potassium to flow in.

Muscarinic Ach receptors have muscarine as an agonist, and work relatively slower because they are not ion channels, they are g-protein coupled receptors.

10
Q

How do nicotinic Ach receptors generate an excitatory post-synaptic potential?

A

They are highly permeable to both Na and K+, but moreso to Na. This lets the membrane go towards 0mV (sodium’s equilibrium potential is +55mV), serving as the excitatory signal on a dendrite, cell body, or neuromuscular junction.