Question 1

The efficacy of synaptic transmission can change. What best represents synaptic facilitation?
A) A long-term increase in the number of synaptic contacts onto a postsynaptic neuron
B) An increase in the postsynaptic response to successive presynaptic action potentials
C) A decrease in the postsynaptic response to successive presynaptic action potentials
D) A decrease in the amplitude of the presynaptic action potential

Accepted Answer

Synaptic facilitation is an increase in the postsynaptic response, or EPSP to successive action potentials in the presynaptic neuron (choice b). Facilitation is not a long-term change in synaptic strength, so choice (a) is not the best answer. Both (c) and (d) are incorrect as facilitation is an increase in the response, not a decrease

Question 2

Myasthenia gravis is an autoimmune neuromuscular disease that results in muscle weakness caused by circulating antibodies that block acetylcholine receptors. People with the disease are treated with acetylcholinesterase (AChase) inhibitors or immunosuppressants. Why do AChase inhibitors work?

Accepted Answer

AChase breaks down and inactivates ACh once it is released into the synaptic cleft. In myasthenia gravis some of the receptors are blocked so increasing the amount of ACh in the cleft increases the probability that the transmitter can bind to the few receptors that are there.

Question 3

Why do you think there are so many types of presynaptic proteins involved in neurotransmitter release?

Accepted Answer

This is a thought question with many possible answers. Reasons could include regulation of neurotransmitter release. Neurotransmission should occur when it is needed. If it occurs at other times this can lead to incorrect information transfer. Neurotransmission must be tightly regulated, but also be able to be modified as the activity of the neuron must change frequently and rapidly depending on the current state of the neuron. Many of the proteins are there to make sure everything is in the right place. For example, some proteins make sure vesicles are located next to Ca²⁺ channels to make sure synaptic transmission is efficient.

Question 4

What are the two major/most common neurotransmitters in the vertebrate CNS?
A) GABA and acetylcholine
B) Glycine and acetylcholine
C) GABA and glutamate
D) GABA and glycine

Accepted Answer

Although acetylcholine and glycine are neurotransmitters in the vertebrate CNS, GABA, and glutamate are the two most common transmitters.

Question 5

Describe, in general terms, experiments that show that Ca²⁺ is both necessary and sufficient for neurotransmitter release. Start with the assumption that you are recording from the squid giant synapse in which you can stimulate the presynaptic neuron and record the response in the postsynaptic neuron. State which experiment shows necessity and which shows sufficiency.

Accepted Answer

The answer of Describe, in general terms, experiments that show...

Question 6

A series of critical experiments showed the properties of chemical synaptic transmission at the neuromuscular junction. One of these is shown in Figure Q3-1 in which the voltage across the membrane was recorded with an intracellular electrode.  Figure Q3-1
A. What happened when the motor axon was stimulated?
B. The investigators then applied ACh to the muscle via iontophoresis in the presence of TTX. Why did they use TTX?
C. The elicited response of ACh iontophoresis was similar to nerve stimulation. What did this tell the investigators?

Accepted Answer

The answer of A series of critical experiments showed the...

Question 7

What mechanisms are used to move neurotransmitter back into vesicles? Select all that apply. A) A Na⁺ chemical gradient B) A proton gradient C) ATP D) A co-transporter

Accepted Answer

C,D
All the choices are correct.

Question 8

Syt1 point mutation is a point mutation in synaptotagmin-1. How did the experiment shown in Figure Q3-12 show that synaptotagmin was probably the Ca²⁺ sensor? Figure Q3-12 B. What would the synaptotagmin-1 mutant response look like if synaptotagmin was not the Ca²⁺ sensor?

Accepted Answer

The answer of Syt1 point mutation is a point mutation...

Question 9

Put the following in the correct order. A. Neurotransmitter release B. Ca²⁺ entry into the presynaptic terminal C. Axonal action potential D. Fusion of synaptic vesicle with the presynaptic plasma membrane E. Opening of voltage-gated Ca²⁺ channels F. Depolarization of the presynaptic terminal

Accepted Answer

The answer of Put the following in the correct order.
A....

Question 10

Figure Q3-6 is from an experiment that helped show that neurotransmitter release is triggered by presynaptic Ca²⁺. In panel A, the presynaptic membrane potential was clamped at -25mV. Figure Q3-6 A. How did they know Ca²⁺ entered the presynaptic neuron? B. What happened in the postsynaptic neuron? C. In panel B, the presynaptic membrane potential was clamped at -50mV. Why was there no net current during the presynaptic depolarization? D. Why was there a current after the presynaptic potential was clamped back to -70mV? E. What happened to the delay in postsynaptic current with the +50mV presynaptic depolarization?

Accepted Answer

The answer of Figure Q3-6 is from an experiment that...

Question 11

The presynaptic active zone must line-up with the postsynaptic density. What is one molecular mechanism that contributes to this alignment?

Accepted Answer

The answer of The presynaptic active zone must line-up with...

Question 12

Which protein is the Ca²⁺ sensor in synaptic transmission? A) Synapsin B) Munc18 C) Synaptotagmin D) Synaptobrevin

Accepted Answer

The Ca²⁺ sensor in synaptic transmission is referring to the calcium sensor protein complex that is responsible for triggering neurotransmitter release. This complex includes the calcium binding protein synaptotagmin, which is the best choice among the given options. Synapsin and Munc18 are involved in regulating the release of neurotransmitters rather than directly sensing calcium. Synaptobrevin is a vesicle-associated membrane protein that plays a role in vesicle fusion with the presynaptic membrane.

Question 13

Flies with the Shibire mutant become paralyzed at high temperatures as this destabilizes dynamin. Why would this result in paralysis? Select all that apply.
A) Actin-myosin is disrupted in muscles and they cannot contract.
B) Vesicle release is blocked.
C) Vesicle recycling is blocked.
D) Synaptic vesicles are depleted in the presynaptic terminal.

Accepted Answer

Dynamin helps move endocytosed vesicles from the presynaptic membrane. If dynamin is destabilized it would block vesicle recycling (choice c) because endocytosis would be blocked. Because recycling is blocked synaptic vesicles in the membrane would eventually become depleted since they could not be restored (choice d). Choice (a) is incorrect as dynamin is not involved in muscle contraction. Vesicle release is not blocked because vesicles can still be released. Vesicles can still fuse with the presynaptic membrane; it is only endocytosis that is blocked.

Question 14

What mechanisms are used to clear neurotransmitters from the synaptic cleft? Select all that apply.
A) Degradation by enzymes
B) Reuptake by co-transporters
C) Transporters on glia
D) Diffusion
E) All of above

Accepted Answer

All of the choices are correct. ACh is degraded by the enzyme acetylcholinesterase. Transmitters like dopamine are taken back up into the presynaptic membrane by co-transporters that use the electrochemical gradient of an ion to provide the energy to transport the transmitter across the presynaptic membrane. Glutamate is taken up by glia. Many molecules diffuse away from the synapse which decreases their concentration and action

Question 15

What is the current known role of complexin in synaptic transmission? A) Complexin makes sure vesicles are near Ca²⁺ channels. B) Complexin binds vesicles to scaffolding proteins in the presynaptic membrane. C) Complexin clamps the SNARE complex in an intermediate step prior to vesicle fusion. D) Complexin is required for presynaptic Ca²⁺ channels to open.

Accepted Answer

The RIMs help place Ca²⁺ channels near vesicles. For (b), complexin binds the SNARE complex, not scaffolding proteins. A depolarization is required for most presynaptic calcium channels to open.

Question 16

What is a miniature end-plate potential (mEPP)? Select all that apply.
A) The change in postsynaptic potential at a very small muscle
B) Spontaneous postsynaptic responses in the absence of a presynaptic action potential
C) Small postsynaptic responses of a unitary size, or multiples of that size
D) The change in postsynaptic potential to a very small action potential

Accepted Answer

(a) is not correct as you can have mEPPs in all muscles, not just small ones. (d) is not correct as action potentials, in general, are consistent in their amplitude. Both (b) and (c) are correct. mEPPs are small, discrete postsynaptic responses to multiple packets of neurotransmitters released from vesicles.

Question 17

Figure Q3-4 documents the quantal release of neurotransmitter. Figure Q3-4 A. The investigators stimulated the nerve in low-Ca²⁺ and high-Mg²⁺ saline so that they had many failures with nerve stimulation. Why was the presence of failures so important? B. In the top trace, there were three motor nerve stimulations that occurred at the arrow. Why is the flat trace flat and, based on what we know now, what is the reason that the other two traces are multiples of each other? C. The investigators compared the evoked EPPs in low Ca²⁺/high Mg²⁺ saline to spontaneous EPPs (mEPP). What did they find (see figures on the right) and what did they conclude? D. Based on the findings in this figure, what did they conclude about transmitter release in an evoked EPP in normal saline?

Accepted Answer

The answer of Figure Q3-4 documents the quantal release of...

Question 18

What is quantal release of neurotransmitter?
A) Release of neurotransmitter in discrete units
B) Release of one neurotransmitter molecule at a time
C) Release of transmitter onto extrasynaptic receptors

Accepted Answer

is correct. Most neurotransmitters are released in discrete units or packets. Graded release of neurotransmitter with a graded change in the presynaptic membrane (like in the retina). Neurotransmitters are packaged and released from vesicles, so (c) is not correct. Although extrasynaptic transmitter release is probably quantal, this is not the correct answer.

Question 19

What are the three main SNARE proteins?
A) Synapsin, SNAP-25, synaptotagmin
B) Synapsin, synaptobrevin and synaptotagmin
C) SNAP-25, syntaxin and synaptobrevin
D) SNAP-25, synaptotagmin, synaptobrevin

Accepted Answer

Synaptotagmin is the Ca²⁺ sensor and synapsin regulates the size of the releasable pool of vesicles.

Question 20

When a depolarization occurs in the presynaptic terminal and Ca²⁺ channels open there is a large global rise in Ca²⁺ concentration. Defend your answer.

Accepted Answer

Most Ca²⁺ channels are located next to vesicles in the active zone of the presynaptic membrane. When Ca²⁺ channels open there are local increases in Ca²⁺, or microdomains in the presynaptic terminal with a large increase in calcium concentration.

Quiz 3: Signaling Across Synapses

The efficacy of synaptic transmission can change. What best represents synaptic facilitation?

Myasthenia gravis is an autoimmune neuromuscular disease that results in muscle weakness caused by circulating antibodies that block acetylcholine receptors. People with the disease are treated with acetylcholinesterase (AChase) inhibitors or immunosuppressants. Why do AChase inhibitors work?

Why do you think there are so many types of presynaptic proteins involved in neurotransmitter release?

What are the two major/most common neurotransmitters in the vertebrate CNS?

What mechanisms are used to move neurotransmitter back into vesicles? Select all that apply.

Syt1 point mutation is a point mutation in synaptotagmin-1. How did the experiment shown in Figure Q3-12 show that synaptotagmin was probably the Ca²⁺ sensor? Figure Q3-12 B. What would the synaptotagmin-1 mutant response look like if synaptotagmin was not the Ca²⁺ sensor?

Put the following in the correct order. A. Neurotransmitter release B. Ca²⁺ entry into the presynaptic terminal C. Axonal action potential D. Fusion of synaptic vesicle with the presynaptic plasma membrane E. Opening of voltage-gated Ca²⁺ channels F. Depolarization of the presynaptic terminal

The presynaptic active zone must line-up with the postsynaptic density. What is one molecular mechanism that contributes to this alignment?

Which protein is the Ca²⁺ sensor in synaptic transmission?

Flies with the Shibire mutant become paralyzed at high temperatures as this destabilizes dynamin. Why would this result in paralysis? Select all that apply.

What mechanisms are used to clear neurotransmitters from the synaptic cleft? Select all that apply.

What is the current known role of complexin in synaptic transmission?

What is a miniature end-plate potential (mEPP) ? Select all that apply.

What is quantal release of neurotransmitter?

What are the three main SNARE proteins?

When a depolarization occurs in the presynaptic terminal and Ca²⁺ channels open there is a large global rise in Ca²⁺ concentration. Defend your answer.

Quiz 3: Signaling Across Synapses

The efficacy of synaptic transmission can change. What best represents synaptic facilitation?

Myasthenia gravis is an autoimmune neuromuscular disease that results in muscle weakness caused by circulating antibodies that block acetylcholine receptors. People with the disease are treated with acetylcholinesterase (AChase) inhibitors or immunosuppressants. Why do AChase inhibitors work?

Why do you think there are so many types of presynaptic proteins involved in neurotransmitter release?

What are the two major/most common neurotransmitters in the vertebrate CNS?

What mechanisms are used to move neurotransmitter back into vesicles? Select all that apply.

Syt1 point mutation is a point mutation in synaptotagmin-1. How did the experiment shown in Figure Q3-12 show that synaptotagmin was probably the Ca2+ sensor? Figure Q3-12 B. What would the synaptotagmin-1 mutant response look like if synaptotagmin was not the Ca2+ sensor?

Put the following in the correct order. A. Neurotransmitter release B. Ca2+ entry into the presynaptic terminal C. Axonal action potential D. Fusion of synaptic vesicle with the presynaptic plasma membrane E. Opening of voltage-gated Ca2+ channels F. Depolarization of the presynaptic terminal

The presynaptic active zone must line-up with the postsynaptic density. What is one molecular mechanism that contributes to this alignment?

Which protein is the Ca2+ sensor in synaptic transmission?

Flies with the Shibire mutant become paralyzed at high temperatures as this destabilizes dynamin. Why would this result in paralysis? Select all that apply.

What mechanisms are used to clear neurotransmitters from the synaptic cleft? Select all that apply.

What is the current known role of complexin in synaptic transmission?

What is a miniature end-plate potential (mEPP) ? Select all that apply.

What is quantal release of neurotransmitter?

What are the three main SNARE proteins?

When a depolarization occurs in the presynaptic terminal and Ca2+ channels open there is a large global rise in Ca2+ concentration. Defend your answer.

Syt1 point mutation is a point mutation in synaptotagmin-1. How did the experiment shown in Figure Q3-12 show that synaptotagmin was probably the Ca²⁺ sensor? Figure Q3-12 B. What would the synaptotagmin-1 mutant response look like if synaptotagmin was not the Ca²⁺ sensor?

Put the following in the correct order. A. Neurotransmitter release B. Ca²⁺ entry into the presynaptic terminal C. Axonal action potential D. Fusion of synaptic vesicle with the presynaptic plasma membrane E. Opening of voltage-gated Ca²⁺ channels F. Depolarization of the presynaptic terminal

Which protein is the Ca²⁺ sensor in synaptic transmission?

When a depolarization occurs in the presynaptic terminal and Ca²⁺ channels open there is a large global rise in Ca²⁺ concentration. Defend your answer.