Chapter 13: Release of Neurotransmitters

Test Bank

Type: multiple choice question

Title: Chapter 13 - Question 01

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?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what the relation is between action potential amplitude and transmitter release

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 02

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what the relation is between action potential amplitude and transmitter release

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 03

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what synaptic delay is and what accounts for it.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 04

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what synaptic delay is and what accounts for it.

Bloom’s Level: 1. Remembering

a. 100 milliseconds

b. 10 milliseconds

c. 0.5 milliseconds

d. 10 microseconds

e. 0.5 microseconds

Type: multiple choice question

Title: Chapter 13 - Question 05

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Describe the role of calcium channels in transmitter release.

Bloom’s Level: 4. Analyzing

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

Type: multiple choice question

Title: Chapter 13 - Question 06

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?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Describe the role of calcium channels in transmitter release.

Bloom’s Level: 4. Analyzing

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.

Type: multiple choice question

Title: Chapter 13 - Question 07

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?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Describe the role of calcium channels in transmitter release.

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 08

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?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Describe the role of calcium channels in transmitter release.

Bloom’s Level: 4. Analyzing

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.

Type: multiple choice question

Title: Chapter 13 - Question 09

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

Feedback: Subhead: Characteristics of Transmitter Release
Learning Objective: Describe the role of calcium channels in transmitter release.

Bloom’s Level: 4. Analyzing

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.

Type: multiple choice question

Title: Chapter 13 - Question 10

10. What is a microdomain of presynaptic calcium ions?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Distinguish between calcium nanodomains and microdomains.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 11

11. What is a nanodomain of presynaptic calcium ions?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Distinguish between calcium nanodomains and microdomains.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 12

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Distinguish between calcium nanodomains and microdomains.

Bloom’s Level: 5. Evaluating

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

Type: multiple choice question

Title: Chapter 13 - Question 13

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Distinguish between calcium nanodomains and microdomains.

Bloom’s Level: 1. Remembering

a. 100 nM

b. 1µM

c. 100 µM

d. 500 µM

e. 1 mM

Type: multiple choice question

Title: Chapter 13 - Question 14

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

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what presynaptic autoreceptors are.

Bloom’s Level: 3. Applying

a. presynaptic autoreceptors.

b. postsynaptic autoreceptors.

c. presynaptic calcium channels.

d. presynaptic sodium channels.

e. postsynaptic ionotropic receptors.

Type: multiple choice question

Title: Chapter 13 - Question 15

15. What is the definition of an autoreceptor?

Feedback: Subhead: Characteristics of Transmitter Release

Learning Objective: Explain what presynaptic autoreceptors are.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 16

16. What is the definition of quantal size?

Feedback: Subhead: Quantal Release

Learning Objective: Define quanta, quantum content, and quantal size.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 17

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

Feedback: Subhead: Quantal Release

Learning Objective: Define quanta, quantum content, and quantal size.

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 18

18. How does the actylcholine receptor antagonist curare affect mEPPs?

Feedback: Subhead: Quantal Release

Learning Objective: Discuss the evidence that showed that spontaneous miniature end plate potentials (MEPPs) are produced by multimolecular ACh quanta rather than by single ACh molecules.

Bloom’s Level: 5. Evaluating

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.

Type: multiple choice question

Title: Chapter 13 - Question 19

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

Feedback: Subhead: Quantal Release

Learning Objective: Discuss the evidence that showed that spontaneous miniature end plate potentials (MEPPs) are produced by multimolecular ACh quanta rather than by single ACh molecules.

Bloom’s Level: 6. Creating

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.

Type: multiple choice question

Title: Chapter 13 - Question 20

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

Feedback: Subhead: Quantal Release

Learning Objective: Discuss the evidence that showed that spontaneous miniature end plate potentials (MEPPs) are produced by multimolecular ACh quanta rather than by single ACh molecules.

Bloom’s Level: 4. Analyzing

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.

Type: multiple choice question

Title: Chapter 13 - Question 21

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

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 5. Evaluating

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.

Type: multiple choice question

Title: Chapter 13 - Question 22

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

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 5. Evaluating

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.

Type: multiple choice question

Title: Chapter 13 - Question 23

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?

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 24

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

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 6. Creating

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.

Type: multiple choice question

Title: Chapter 13 - Question 25

25. When applying statistical methods to analyze transmitter release, what does the term “n” represent in the binomial theory?

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 26

26. When applying statistical methods to analyze transmitter release, what does the term “p” represent in the binomial theory?

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 27

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?

Feedback: Subhead: Quantal Release

Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 5. Evaluating

a. 1

b. 10

c. 100

d. 500

e. 1,000

Type: multiple choice question

Title: Chapter 13 - Question 28

28. What is the definition of a quantum of transmitter?

Feedback: Subhead: Quantal Release

Learning Objective: Describe the experimental setup by which researchers determined the number of ACh molecules in a quantum.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 29

29. Which of the following occurs at active zones?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Explain what the active zone of a nerve terminal is and what role it plays in transmitter release.

Bloom’s Level: 2. Understanding

a. Synaptic protein translation

b. Mitochondrial generation of ATP

c. Neurotransmitter synthesis

d. Action potential generation

e. Vesicle exocytosis

Type: multiple choice question

Title: Chapter 13 - Question 30

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.

Bloom’s Level: 5. Evaluating

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.

Type: multiple choice question

Title: Chapter 13 - Question 31

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.

Bloom’s Level: 5. Evaluating

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.

Type: multiple choice question

Title: Chapter 13 - Question 32

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 33

33. What is the calcium sensor for synaptic vesicle exocytosis?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.

Bloom’s Level: 3. Analyzing

a. Complexin

b. SNAP-25

c. Syntaxin

d. Synaptobrevin

e. Synaptotagmin

Type: multiple choice question

Title: Chapter 13 - Question 34

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.

Bloom’s Level: 2. Understanding

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.

Type: multiple choice question

Title: Chapter 13 - Question 35

35. What is kiss-and-run exocytosis?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the kiss-and-run mode of exocytosis.

Bloom’s Level: 2. Understanding

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

Type: multiple choice question

Title: Chapter 13 - Question 36

36. What are the different forms of endocytosis?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the two basic pathways by which depleted vesicles are retrieved and recycled.

Bloom’s Level: 1. Remembering

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

Type: multiple choice question

Title: Chapter 13 - Question 37

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the two basic pathways by which depleted vesicles are retrieved and recycled.

Bloom’s Level: 4. Analyzing

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.

Type: multiple choice question

Title: Chapter 13 - Question 38

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

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the three different types of vesicle pools found in the nerve terminal.

Bloom’s Level: 1. Remembering

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

Type: multiple choice question

Title: Chapter 13 - Question 39

39. What is the readily releasable pool of vesicles?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the three different types of vesicle pools found in the nerve terminal.

Bloom’s Level: 3. Applying

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

Type: multiple choice question

Title: Chapter 13 - Question 40

40. What is the recycling pool of vesicles?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the three different types of vesicle pools found in the nerve terminal.

Bloom’s Level: 3. Applying

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

Type: multiple choice question

Title: Chapter 13 - Question 41

41. What is the reserve pool of vesicles?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the three different types of vesicle pools found in the nerve terminal.

Bloom’s Level: 3. Applying

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

Type: multiple choice question

Title: Chapter 13 - Question 42

42. In which vesicle pool does newly synthesized neurotransmitter become loaded?

Feedback: Subhead: Vesicles and Transmitter Release

Learning Objective: Describe the three different types of vesicle pools found in the nerve terminal.

Bloom’s Level: 4. Analyzing

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

Type: essay/short answer question

Title: Chapter 13 - Question 43

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?

Feedback: This result indicates that the normal fluxes of sodium and potassium ions responsible for the action potential are not necessary for transmitter release; only depolarization is required. This depolarization is all that is required to open voltage-gated calcium channels, and the resultant calcium influx into the nerve terminal is both necessary and sufficient for transmitter release.

Subhead: Characteristics of Transmitter Release
Learning Objective: Explain what the relation is between action potential amplitude and transmitter release.
Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 13 - Question 44

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

Feedback: Caged calcium is a photolabile (sensitive to light) calcium chelator, which releases bound, or “caged,” calcium upon illumination. This provides a means of producing a transient increase in intracellular calcium in the presynaptic terminal, in the absence of any change in membrane potential (i.e. without an action potential).

Subhead: Characteristics of Transmitter Release
Learning Objective: Describe the role of calcium channels in transmitter release.
Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 45

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.

Feedback: If an experimenter compares the effects of two different buffers (EGRTA and BAPTA) that each have similar potency at binding calcium, but different speeds, one can determine which buffer can compete with the transmitter release process for binding calcium ions. If the slower buffer is effective, this is interpreted to mean that the calcium entry sites and the transmitter release process are far apart. If only the faster buffer can block transmitter release, this is interpreted to mean that the sites of calcium entry and the transmitter release process are very close to one another.

Subhead: Characteristics of Transmitter Release
Learning Objective: Distinguish between calcium nanodomains and microdomains.
Bloom’s Level: 6. Creating

Type: essay/short answer question

Title: Chapter 13 - Question 46

46. How do presynaptic autoreceptors regulate transmitter release?

Feedback: Presynaptic autoreceptors are G protein-coupled receptors on the presynaptic terminals which, when activated by released transmitter, act in turn to inhibit further release. For example, presynaptic muscarinic cholinergic (M2) receptors at the mouse NMJ are continually exposed to a resting concentration of ACh, which produces tonic inhibition of the release mechanism. In this case, the ACh binding affinity for these receptors is voltage-dependent, such that depolarization of the nerve terminal is thought to reduce the binding affinity of the M2 receptors, thereby relieving tonic inhibition of release. Upon repolarization, the inhibitory action of the M2 receptors is restored, so that the release is terminated even though the calcium concentration in the region may still be elevated.

Subhead: Characteristics of Transmitter Release
Learning Objective: Explain what presynaptic autoreceptors are.
Bloom’s Level: 5. Evaluating

Type: essay/short answer question

Title: Chapter 13 - Question 47

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

Feedback: The quantum content is very different at different synapses. At the neuromuscular junction, where there is only one nerve terminal on each muscle fiber, the quantum content is 200-300. In autonomic ganglia, synapses have quantum contents of 2-20, and in the central nervous system where most postsynaptic cells integrate the input from thousands of synapses, most of these small synapses have a quantum content of about 1.

Subhead: Quantal Release
Learning Objective: Define quanta, quantum content, and quantal size.
Bloom’s Level: 1. Remembering

Type: essay/short answer question

Title: Chapter 13 - Question 48

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?

Feedback: Patch electrode recordings demonstrated directly that the amount of current that flows through an individual ACh receptor will produce a potential change in the muscle fiber of approximately 1 μV. Thus, based on the amplitude of mEPPs (about 1.3 mV at the frog NMJ), we can estimate that a mEPP is produced by the opening of about 1300 ACh receptors. In addition, gradually blocking postsynaptic receptors gradually reduced the size of mEPPs, indicated that the potentials were produced by the spontaneous release of discrete amounts of ACh from the nerve terminal and ruled out the possibility that they might be due to single ACh molecules.

Subhead: Quantal Release
Learning Objective: Discuss the evidence that showed that spontaneous miniature end plate potentials (MEPPs) are produced by multimolecular ACh quanta rather than by single ACh molecules.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 13 - Question 49

49. Explain the quantum hypothesis.

Feedback: The quantum hypothesis states that transmitter is released in multimolecular packets called quanta. Further, single quantal events observed to occur spontaneously (recorded as mEPPs) also represent the building blocks for the synaptic potentials evoked by presynaptic action potentials. A presynaptic action potential causes the release of many quanta, or packets of transmitter.

Subhead: Quantal Release
Learning Objective: Explain what the quantum hypothesis is.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 50

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

Feedback: The postsynaptic receptor density at different synapses varies over a wide range. For example, at the neuromuscular junction, receptors are packed at high density (~10,000/μm²) throughout a large expanse of postsynaptic membrane, providing an essentially limitless sea of receptors for each quantum of transmitter. At a typical hippocampal synapse, however, the estimated postsynaptic receptor density is much lower (~2800/μm²), and the area occupied by postsynaptic membrane is very small (0.04 μm²). Thus, fewer than 100 postsynaptic receptors may be available for activation by a single quantum.

Subhead: Quantal Release
Learning Objective: Explain why the number of receptors activated by a quantum varies among synapses.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 51

51. What is an “active zone”?

Feedback: A collection of proteins at a defined spot in the nerve terminal (observed as a density in electron micrographs) where synaptic vesicles can fuse with the nerve terminal plasma membrane to release transmitter. The active zone is considered the “active” location in the nerve terminal where calcium entry through voltage-gated calcium channels triggers transmitter release.

Subhead: Vesicles and Transmitter Release
Learning Objective: Explain what the active zone of a nerve terminal is and what role it plays in transmitter release.
Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 52

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

Feedback: The use of the freeze fracture technique, in which muscle was quick-frozen within milliseconds after a single shock to the motor nerve, and then prepared for freeze-fracture electron microscopy. Using this method, the frozen tissue could be fractured along the membrane bilayer to reveal the proteins that line the active zone and the appearance of “holes” in the freeze fracture image at sites where synaptic vesicles fused with the plasma membrane. Such holes were not present when the tissue was not stimulated before freezing.

Subhead: Vesicles and Transmitter Release
Learning Objective: Explain what the active zone of a nerve terminal is and what role it plays in transmitter release.
Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 53

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

Feedback: The t-SNARE syntaxin is held in a closed state by the regulatory protein Munc 18-1, and in that configuration is unable to interact with other SNARE proteins. Docking is followed by a priming stage in which Munc 13 interacts with the Munc 18-1/syntaxin complex to allow syntaxin to enter its open state. Once in its open state, syntaxin can form the SNARE complex four helix bundle by binding to synaptobrevin and SNAP-25.

Subhead: Vesicles and Transmitter Release
Learning Objective: Describe how synaptic vesicles release their contents by exocytosis.
Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 13 - Question 54

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?

Feedback: To prevent inactivation of calcium channels at these synapses during prolonged and graded activation, calcium entry is mediated by CaV1 channels (known generically as L-type channels for their Long openings with little or no inactivation). L channels allow sustained calcium influx during sustained depolarization, unlike the Cav2 channels types at fast synapses in other areas of the nervous system which inactivate more quickly.

Subhead: Vesicles and Transmitter Release
Learning Objective: Explain what ribbon synapses are and name two types of cells in which they occur.
Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 13 - Question 55

55. How do calcium ions trigger synaptic vesicle exocytosis?

Feedback: Calcium ions entering the nerve terminal through voltage-activated calcium channels binds to synaptotagmin, which in turn binds to the SNARE complex, displacing

complexin and initiating pore formation. This is the first step that leads to exocytosis.

Subhead: Vesicles and Transmitter Release
Learning Objective: Describe what happens to vesicles after they release their contents.
Bloom’s Level: 5. Evaluating

Type: essay/short answer question

Title: Chapter 13 - Question 56

56. What is a synaptic ribbon?

Feedback: A synaptic ribbon is an intracellular organelle within some retinal neurons that tethers large numbers of vesicles near the presynaptic active zone and is composed largely of the protein RIBEYE. Its structure is anchored to the active zone and extends from the synaptic membrane into the cytoplasm.

Subhead: Vesicles and Transmitter Release
Learning Objective: Describe the two basic pathways by which depleted vesicles are retrieved and recycled.
Bloom’s Level: 5. Evaluating

Type: essay/short answer question

Title: Chapter 13 - Question 57

57. What are the steps in “bulk endocytosis”?

Feedback: After particularly intense stimulation, large portions of the nerve terminal membrane pinch in creating cisterns, presumably because the process of clathrin-mediated endocytosis can’t keep up with exocytosis at this high release rate. Clathrin-coated vesicles are then budded off from large, uncoated pits and cisterns that form during “bulk endocytosis”. After retrieval, vesicles lose their coats and are returned to the vesicle pools for loading and re-use.

Subhead: Vesicles and Transmitter Release
Learning Objective: Describe the two basic pathways by which depleted vesicles are retrieved and recycled.
Bloom’s Level: 6. Creating