Multiple Choice
At the frog neuromuscular junction, when you block voltage-gated sodium channels selectively in muscle (but not nerve) , and then record EPPs (using the microelectrode technique) in response to repeated low frequency nerve stimulation, you see EPPs that are very large (each depolarizes muscle membrane above resting potential to about -30 mV) , but these EPPS do not fluctuate significantly when you compare the size of each EPP. Why do these EPPs not vary significantly in amplitude?
A) This very large EPP is above threshold and an action potential is evoked which is all-or-none and thus does not show amplitude fluctuations.
B) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the voltage-gated sodium channel.
C) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the acetylcholine receptor channel.
D) The very large EPP is caused by the release of a fixed large number of transmitter molecules that are not packaged into vesicles.
E) The very large EPP is caused by the release of a fixed number of synaptic vesicles released and this number of vesicles does not change with each stimulation.
Correct Answer:

Verified
Correct Answer:
Verified
Q22: What is the principal excitatory transmitter in
Q23: What is the "synaptic cleft"?<br>A) The nerve
Q24: What is the reversal potential for an
Q25: How do acetycholinesterase drugs (i.e. physostigmine) alter
Q26: How do transmitters act on the postsynaptic
Q28: The reversal potential for the nicotinic acetylcholine
Q29: How does the technique called ionophoresis work?<br>A)
Q30: Describe the mechanism by which auto-inhibition alters
Q31: What is an endplate potential?<br>A) The membrane
Q32: Why do single channel measurements of acetylcholine