Question 1

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

Accepted Answer

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. 
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 2

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?

Accepted Answer

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. 
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.

Question 3

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?

Accepted Answer

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. 
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 4

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

Accepted Answer

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. 
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 5

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

Accepted Answer

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. 
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 6

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

Accepted Answer

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. 
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 7

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

Accepted Answer

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. 
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 8

What is the definition of a quantum of transmitter?

Accepted Answer

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 
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 9

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

Accepted Answer

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. 
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 10

What is the definition of an autoreceptor?

Accepted Answer

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 
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 11

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

Accepted Answer

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

Question 12

What is the calcium sensor for synaptic vesicle exocytosis?

Accepted Answer

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

Question 13

What are the steps in "bulk endocytosis"?

Accepted Answer

After particularly intense stimulation,

Question 14

What is a nanodomain of presynaptic calcium ions?

Accepted Answer

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 
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 15

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

Accepted Answer

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 
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 16

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

Accepted Answer

The postsynaptic receptor density at dif

Question 17

How do presynaptic autoreceptors regulate transmitter release?

Accepted Answer

Presynaptic autoreceptors are G protein-

Exam 13: Release of Neurotransmitters

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

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?

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?

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

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

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

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

What is the definition of a quantum of transmitter?

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

What is the definition of an autoreceptor?

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

What is the calcium sensor for synaptic vesicle exocytosis?

What are the steps in "bulk endocytosis"?

What is a nanodomain of presynaptic calcium ions?

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

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

How do presynaptic autoreceptors regulate transmitter release?

Principles of Signaling and Organization

Signaling in the Visual System

Functional Architecture of the Visual Cortex

Ion Channels and Signaling

Structure of Ion Channels

Ionic Basis of the Resting Potential

Ionic Basis of the Action Potential

Electrical Signaling in Neurons

Ion Transport Across Cell Membranes

Properties and Functions of Neuroglial Cells

Mechanisms of Direct Synaptic Transmission

Indirect Mechanisms of Synaptic Transmission

Neurotransmitters in the Central Nervous System

Transmitter Synthesis, Storage, Transport, and Inactivation

Synaptic Plasticity

The Molecular and Cellular Biology of Synaptic Plasticity

Mechanisms of Extrasynaptic Communication

Autonomic Nervous System

Walking, Flying, and Swimming: Cellular Mechanisms of Sensorimotor Behavior in Invertebrates

Sensory Transduction

Transduction and Transmission in the Retina

Touch, Pain, and Texture Sensation

Auditory and Vestibular Sensation

Constructing Perception

Initiation and Control of Coordinated Muscular Movements

Development of the Nervous System

Critical Periods in Sensory Systems

Regeneration and Repair of Synaptic Connections After Injury

Appendix

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