Deck 13: Release of Neurotransmitters

Question 1

What explains why the magnitude of transmitter released from nerve terminals decreases rapidly as the action potential amplitude is reduced form about 75 mV to about 45 mV?

A) The number of presynaptic sodium channels activated decreases.
B) The number of presynaptic potassium channels activated decreases.
C) The number of presynaptic calcium channels activated decreases.
D) The number of presynaptic chloride channels activated decreases.
E) The number of postsynaptic transmitter receptor channels activated decreases.

Answer 1

C

Question 2

What explains why there is a threshold depolarization of about 45 mV above resting membrane potential before any transmitter release occurs?

A) This is the magnitude of depolarization required to activate presynaptic voltage gated sodium channels.
B) This is the magnitude of depolarization required to activate presynaptic voltage gated potassium channels.
C) This is the magnitude of depolarization required to activate a presynaptic action potential.
D) This is the magnitude of depolarization required to activate presynaptic voltage-gated calcium channels.
E) This is the magnitude of depolarization required to activate a postsynaptic action potential.

Answer 2

D

Question 3

What process at chemical synapses takes the most time and contributes the most to the synaptic delay?

A) Diffusion of transmitter across the synaptic cleft
B) The transmitter release process in the nerve terminal
C) The binding of transmitter to postsynaptic ionotropic receptors
D) The opening of channels in postsynaptic ionotropic receptors
E) The opening of presynaptic calcium channels in response to an action potential

Answer 3

E

Question 4

What is the synaptic delay at a synapse that uses chemical transmitters at room temperature?

A) 100 milliseconds
B) 10 milliseconds
C) 0.5 milliseconds
D) 10 microseconds
E) 0.5 microseconds

Question 5

Which is both necessary and sufficient to trigger chemical transmitter release from a presynaptic nerve terminal?

A) A presynaptic action potential
B) An opening of presynaptic sodium channels
C) An opening of presynaptic potassium channels
D) An increase in presynaptic calcium concentration
E) Proton-dependent transport of transmitter into vesicles

Question 6

If an experimenter used the voltage clamp technique to change the presynaptic voltage from -70 mV to +60 mV, what would happen to voltage-gated calcium channels?

A) Voltage-gated calcium channels would open and pass a large amount of inward current.
B) Voltage-gated calcium channels would open and pass a large amount of outward current.
C) Voltage-gated calcium channels would open but no current would pass through the open channel.
D) Voltage-gated calcium channels would not open and therefore, not pass any current.
E) Voltage-gated calcium channels would not open but a large amount of inward current would pass across the membrane.

Question 7

If one would like to use the voltage clamp technique to record presynaptic calcium currents from a nerve terminal, why are tetrodotoxin (TTX) and tetraethylammonium (TEA) used?

A) TTX blocks potassium channels and TEA blocks sodium channels.
B) TTX blocks sodium channels and TEA blocks potassium channels.
C) TTX blocks calcium channels and TEA blocks potassium channels.
D) TTX blocks sodium channels and TEA blocks calcium channels.
E) TTX blocks sodium channels and TEA blocks chloride channels.

Question 8

Why is there a sudden large influx of calcium ions into a nerve terminal when the membrane potential repolarizes from a strong depolarization back to resting membrane potential?

A) The driving force for calcium entry is increased.
B) The driving force for calcium entry is decreased.
C) Calcium channels are opened by the repolarization.
D) Calcium channels are closed by the repolarization.
E) There is no change in the driving force for calcium entry.

Question 9

How does the presence of high concentrations of extracellular magnesium or cadmium ions block transmitter release?

A) Magnesium and cadmium compete with calcium for passage through the presynaptic voltage-gated calcium channel, preventing calcium entry.
B) Magnesium and cadmium compete with sodium for passage through the presynaptic voltage-gated sodium channel.
C) Magnesium and cadmium directly block synaptic vesicle fusion with the plasma membrane.
D) Magnesium and cadmium block presynaptic action potentials.
E) Magnesium and cadmium compete with potassium for passage through the presynaptic voltage-gated potassium channel.

Question 10

What is a microdomain of presynaptic calcium ions?

A) The intracellular calcium ions that fill the presynaptic nerve terminal
B) The intracellular calcium ions that are pumped out of the presynaptic nerve terminal
C) The intracellular calcium ions that diffuse into the synaptic cleft
D) The collected intracellular calcium ions that form around the mouth of a collection of open calcium channels
E) The collected intracellular calcium ions that form around the mouth of a single open calcium channel

Question 11

What is a nanodomain of presynaptic calcium ions?

A) The intracellular calcium ions that fill the presynaptic nerve terminal
B) The intracellular calcium ions that are pumped out of the presynaptic nerve terminal
C) The intracellular calcium ions that diffuse into the synaptic cleft
D) The collected intracellular calcium ions that form around the mouth of a collection of open calcium channels
E) The collected intracellular calcium ions that form around the mouth of a single open calcium channel

Question 12

What is thought to significantly restrict the spread of calcium ions after they enter the nerve terminal through presynaptic calcium channels?

A) The presynaptic calcium channel
B) Calcium buffers and binding proteins (chelators)
C) The activity of potassium channels
D) Calcium binding to synaptotagmin
E) The calcium concentration gradient across the nerve terminal membrane

Question 13

What is the concentration of calcium estimated to be in the presynaptic nerve terminal after a brief train of action potentials?

A) 100 nM
B) 1µM
C) 100 µM
D) 500 µM
E) 1 mM

Question 14

When a chemical transmitter is released from the presynaptic nerve terminal and acts back on the same nerve terminal, it uses

A) presynaptic autoreceptors.
B) postsynaptic autoreceptors.
C) presynaptic calcium channels.
D) presynaptic sodium channels.
E) postsynaptic ionotropic receptors.

Question 15

What is the definition of an autoreceptor?

A) A receptor that is activated automatically with presynaptic action potential activity
B) A receptor that is only activated when the postsynaptic cell is active
C) A presynaptic receptor that binds transmitter molecules released from a postsynaptic cell
D) A presynaptic receptor that binds transmitter molecules released from the same presynaptic nerve terminal
E) A postsynaptic receptor that binds transmitter molecules released from a presynaptic nerve terminal

Question 16

What is the definition of quantal size?

A) The number of molecules of transmitter in one quantum
B) The number of quanta that are released following a presynaptic action potential
C) The number of quanta that are released spontaneously (in the absence of action potentials)
D) The total content of transmitter in the presynaptic nerve terminal
E) The total number of postsynaptic receptors activated after the release of one synaptic vesicle

Question 17

What are the effects of nonquantal release of acetylcholine at the neuromuscular junction?

A) This nonquantal release creates a slow dribble of ACh that has no effects on the postsynaptic muscle cell because it is degraded by acetylcholinesterase.
B) This nonquantal release creates a slow dribble of ACh that depolarizes the postsynaptic muscle cell because it escapes being degraded by acetylcholinesterase.
C) This nonquantal release creates a large amount of ACh that can cause the postsynaptic muscle cell to fire an action potential.
D) This nonquantal release is much less than is released during spontaneous quantal release (mEPPs).
E) Nonquantal release does not occur at the neuromuscular junction.

Question 18

How does the actylcholine receptor antagonist curare affect mEPPs?

A) Curare prolongs the time course of mEPPs.
B) Curare increases the amplitude of mEPPs.
C) Curare prolongs the time course and increases the amplitude of mEPPs.
D) Curare reduces the amplitude or blocks mEPPs.
E) Curare has no effect on mEPPs.

Question 19

What happens to mEPPs when you depolarize the presynaptic nerve terminal membrane by 10-20 mV?

A) There is no change in mEPPs
B) mEPPs increase in amplitude.
C) mEPPs increase in time course.
D) mEPPs increase in amplitude and time course.
E) mEPPs increase in frequency.

Question 20

What happens to miniature endplate potentials (mEPPs) recorded at the frog neuromuscular junction after acetylcholinesterase is blocked by prostigmine?

A) mEPPs decrease in amplitude.
B) mEPPs increase in amplitude and time course.
C) mEPPs do not change in amplitude or time course.
D) mEPPs increase in frequency
E) mEPPs do not occur.

Question 21

If the concentration of extracellular calcium is reduced at the frog neuromuscular synapse, what happens to transmitter release.

A) mEPPs no longer are observed.
B) Transmitter release increases in magnitude.
C) Transmitter release does not change.
D) The quantal size remains the same, but the quantum content is reduced.
E) The quantum content remains the same, but the quantal size is reduced.

Question 22

At the frog NMJ, why does lowering the extracellular calcium and adding extracellular magnesium reduce the amplitude of EPPs?

A) This results in a reduced probability of quantal release of transmitter due to reduced calcium influx.
B) This results in an increased probability of quantal release of transmitter due to increased magnesium influx.
C) This results in a reduced probability of quantal release of transmitter due to a reduced depolarization of the nerve terminal membrane.
D) This results in a reduced probability of quantal release of transmitter due to a increased depolarization of the nerve terminal membrane.
E) This results in a change in the nerve terminal input resistance which changes the magnitude of the EPP without a change in the probability of quantal release of transmitter.

Question 23

At the frog NMJ, why does lowering the extracellular calcium and adding extracellular magnesium not only reduces the amplitude of EPPs on average, but also leads to the occasional failure of the nerve terminal to release transmitter after nerve stimulation?

A) Occasionally the nerve terminal fails to trigger an action potential after nerve stimulation.
B) The reduced calcium and increased magnesium reduces the probability of transmitter release so much that occasionally there is a statistical chance of failure to release any transmitter.
C) The reduced calcium and increased magnesium reduces the probability of transmitter release to zero.
D) The reduced calcium and increased magnesium can also block the postsynaptic acetylcholine receptor.
E) The reduced calcium and increased magnesium increases the activity of the acetylcholinesterase in the synaptic cleft.

Question 24

At the frog NMJ, after lowering the extracellular calcium and adding extracellular magnesium, how are mEPPs affects?

A) There is no change in mEPPs.
B) mEPP amplitude is reduced.
C) mEPP amplitude is increased.
D) mEPP frequency is reduced.
E) mEPP frequency is increased.

Question 25

When applying statistical methods to analyze transmitter release, what does the term "n" represent in the binomial theory?

A) The number of quanta available for release
B) The number of receptors on the postsynaptic membrane
C) The number of synapses
D) The number of calcium channels that open with each action potential
E) The number of number of observations in an experiment

Question 26

When applying statistical methods to analyze transmitter release, what does the term "p" represent in the binomial theory?

A) The probability of transmitter release from the whole nerve terminal
B) The probability of receptors binding transmitter
C) The probability of transmitter release from each release site in one nerve terminal
D) The probability of calcium channel opening during an action potential
E) The probability of action potential generation

Question 27

At a central nervous system neuron that integrates the input from thousands of synapses onto its dendrites, what is the expected average number of quanta released at each synapse?

A) 1
B) 10
C) 100
D) 500
E) 1,000

Question 28

What is the definition of a quantum of transmitter?

A) A single molecule of transmitter
B) The amount of transmitter that is released following a presynaptic action potential
C) The amount of calcium required to trigger transmitter release
D) A multimolecular packet containing about 700 transmitter molecules
E) A multimolecular packet containing about 7000 transmitter molecules

Question 29

Which of the following occurs at active zones?

A) Synaptic protein translation
B) Mitochondrial generation of ATP
C) Neurotransmitter synthesis
D) Action potential generation
E) Vesicle exocytosis

Question 30

How does the addition of 4-aminopyridine (4-AP) to the bathing solution around the neuromuscular junction affect transmitter release?

A) 4-AP blocks sodium channels, preventing action potentials and reducing transmitter release.
B) 4-AP blocks potassium channels, prolonging the duration of action potentials and enhancing transmitter release.
C) 4-AP blocks calcium channels, reducing calcium ion entry and transmitter release.
D) 4-AP enhances potassium channels, shortening the duration of action potentials and reducing transmitter release.
E) 4-AP enhances calcium channels, increasing calcium ion entry and transmitter release.

Question 31

Why are chromaffin cells of the adrenal medulla a good model for studying vesicle release?

A) Chromaffin cells release the same transmitter as the neuromuscular junction.
B) Chromaffin cells contain granules, which are organelles that are analogous to, and the same size as, synaptic vesicles. Therefore, studying granule release is the same as studying synaptic vesicle release.
C) Chromaffin cells contain granules, which are organelles that are analogous to, but much smaller, than synaptic vesicles. Exocytosis of these smaller granules is faster and therefore, easier to study.
D) Chromaffin cells contain granules, which are organelles that are analogous to, but much larger than, synaptic vesicles. Exocytosis of these larger granules is easier to study.
E) Chromaffin cells release transmitter in a nonquantal fashion, without the use of synaptic vesicles.

Question 32

Exocytosis involves the action of three SNARE proteins. What are the names of these three proteins?

A) Synaptotagmin, syntaxin, and SNAP-25
B) Synaptotagmin, synaptobrevin, and SNAP-25
C) Synaptobrevin, syntaxin, and SNAP-25
D) Synaptotagmin, syntaxin, and synaptobrevin
E) Complexin, syntaxin, and SNAP-25

Question 33

What is the calcium sensor for synaptic vesicle exocytosis?

A) Complexin
B) SNAP-25
C) Syntaxin
D) Synaptobrevin
E) Synaptotagmin

Question 34

What do Rab proteins (a family of GTPases) do to assist in the process of exocytosis?

A) Rab proteins are calcium sensors for exocytosis.
B) Rab proteins prepare syntaxin for participation in the SNARE protein four-helix bundle.
C) Rab proteins stabilize the SNARE complex to prevent fusion until calcium ions enter the nerve terminal.
D) Rab proteins target synaptic vesicles to appropriate membrane sites for subsequent docking.
E) Rab proteins are involve in recovering synaptic vesicle membrane after exocytosis.

Question 35

What is kiss-and-run exocytosis?

A) Vesicle pore formation with the plasma membrane followed by full vesicle fusion
B) Vesicles dock with the plasma membrane, but then undock before releasing transmitter
C) Vesicle membrane remains part of the plasma membrane after exocytosis
D) Vesicle pore formation with the plasma membrane that is not followed by full vesicle fusion, but rather by closure of the pore
E) A form of exocytosis that does not release any neurotransmitter

Question 36

What are the different forms of endocytosis?

A) Kiss-and-run, ultra-slow endocytosis, and clathrin-mediated endocytosis
B) Kiss-and-run, bulk endocytosis, ultra-fast endocytosis, and clathrin-mediated endocytosis
C) Kiss-and-run, bulk endocytosis, ultra-slow endocytosis, and clathrin-mediated endocytosis
D) Bulk endocytosis, ultra-fast endocytosis, and clathrin-mediated endocytosis
E) Kiss-and-run, bulk endocytosis, ultra-fast endocytosis, ultra-slow endocytosis, and clathrin-mediated endocytosis

Question 37

When synaptic vesicles collapse into the plasma membrane, and then participate in endocytosis, they

A) pull back into their lumen the soluble contents of the extracellular saline.
B) pull back selectively transmitter from the synaptic cleft.
C) do not pull anything back into the vesicle; they are empty.
D) pull back selectively the breakdown products of transmitter.
E) pull back acetylcholinesterase from the synaptic cleft.

Question 38

What are the three distinct synaptic vesicle pools in the nerve terminal?

A) Docked pool, primed pool, and reserve pool
B) Readily releasable pool, docked pool, and reserve pool
C) Extra pool, recycling pool, and reserve pool
D) Extra pool, readily releasable pool, and reserve pool
E) Readily releasable pool, recycling pool, and reserve pool

Question 39

What is the readily releasable pool of vesicles?

A) Vesicles that are only released during intense prolonged stimulation
B) Vesicles that result from recent endocytosis and are re-filled with transmitter
C) The first vesicles to be released upon stimulation
D) Vesicles that are not depleted rapidly by stimulation
E) Vesicles that are never released with action potential stimulation

Question 40

What is the recycling pool of vesicles?

A) Vesicles that are only released during intense prolonged stimulation
B) Vesicles that result from recent endocytosis and are re-filled with transmitter
C) The first vesicles to be released upon stimulation
D) Vesicles that are not depleted rapidly by stimulation
E) Vesicles that are never released with action potential stimulation

Question 41

What is the reserve pool of vesicles?

A) Vesicles that are only released during intense prolonged stimulation
B) Vesicles that result from recent endocytosis and are re-filled with transmitter
C) The first vesicles to be released upon stimulation
D) Vesicles that are not depleted rapidly by stimulation
E) Vesicles that are never released with action potential stimulation

Question 42

In which vesicle pool does newly synthesized neurotransmitter become loaded?

A) The reserve pool
B) The readily releasable pool
C) The extra pool
D) The readily releasable pool and the reserve pool
E) The recycling pool

Question 43

Why does transmitter release continue to occur after blocking presynaptic sodium channels with the toxin TTX (which blocks the presynaptic action potential) and experimentally depolarizing the nerve terminal?

Question 44

What is caged calcium, and what can it be used for in studies of the nerve terminal?

Question 45

Explain how calcium buffers can be used in experiments on the squid giant synapse to provide information about the proximity of calcium channels to the sites of transmitter secretion.

Question 46

How do presynaptic autoreceptors regulate transmitter release?

Question 47

Is the quantum content the same or different at different types of synapses? Provide examples and explanations.

Question 48

What is the experimental evidence that spontaneous miniature end plate potentials (mEPPs) are produced by the release of many molecules of acetylcholine, rather than a single molecule of acetylcholine?

Question 49

Explain the quantum hypothesis.

Question 50

Why is the number of receptors activated by a single quantum different at different synapses?

Question 51

What is an "active zone"?

Question 52

What is the experimental evidence that synaptic vesicles actually fuse with the plasma membrane during transmitter release?

Question 53

What is the role of Munc-13 in synaptic vesicle exocytosis?

Question 54

What synaptic differences do ribbon synapses at retinal photoreceptors possess that allow them to release transmitter in a graded fashion that varies with illumination?

Question 55

How do calcium ions trigger synaptic vesicle exocytosis?

Question 56

What is a synaptic ribbon?

Question 57

What are the steps in "bulk endocytosis"?