Deck 6: Synapse Formation and Maturation

Question 1

The development of _______ is the first known evolutionary precursor to synapses.

A) transmembrane proteins
B) cell-cell signaling
C) dendritic spines
D) GABA receptors

Answer 1

A

Question 2

The duplication and divergence of many synapse-related genes about 500 million years ago lead to vertebrate synapses

A) functioning differently from invertebrate synapses.
B) developing a wider array of neurotransmitter receptors.
C) being the first to include multiple neurotransmitter receptors.
D) using cell-cell signaling.

Answer 2

B

Question 3

The synaptic cleft is filled with

A) synaptic vesicles.
B) postsynaptic densities.
C) neurotransmitter receptors.
D) extracellular matrix.

Answer 3

D

Question 4

What is the first step in the formation of the synapse?

A) Assembly of synaptic machinery
B) Stabilization of the synapse
C) Adhesive contact between cells
D) Production of neurotransmitters

Question 5

In order to build a synapse, which molecules are necessary to keep cells together?

A) Cadherins
B) Semaphorins
C) Integrins
D) β-catenin

Question 6

If the gene for β-catenin is knocked out, what will happen to synapse development?

A) Adhesion molecules will be anchored too tightly
B) The number of synaptic spines will decrease
C) Synaptic spines will not be pruned
D) Synaptic spines will be over-pruned

Question 7

Fragile X syndrome is caused by too _______ trinucleotide repeats, which results in a(n) _______ in the number of synapses in the brain.

A) few; decrease
B) few; increase
C) many; decrease
D) many; increase

Question 8

In synapse formation, the presynaptic terminal produces _______, which binds to _______ in the postsynaptic terminal to trigger the assembly of neurotransmitter-releasing machinery.

A) neuroligin; neurexin
B) neurexin; neuroligin
C) neuroligin; synaptotagmin
D) neurexin; neuregulin

Question 9

In synaptic transmission, the SNARE complex

A) anchors a vesicle to the presynaptic membrane.
B) releases vesicle contents into the synapse.
C) is a calcium sensor.
D) triggers the fusion of the vesicle and cell membranes.

Question 10

Which protein regulates vesicle fusion in response to Ca²⁺ in the presynaptic axon?

A) Syntaxin
B) SNAP25
C) Synaptobrevin
D) Synaptotagmin

Question 11

From earliest to latest, what is the order of muscle cell development?

A) Myotube, myoblast, myofiber
B) Myoblast, myotube, myofiber
C) Myotube, myofiber, myoblast
D) Myoblast, myofiber, mytotube

Question 12

When happens when a motor neuron axonal growth cone contacts a myotube?

A) The myotube begins expressing acetylcholine receptors.
B) The motor neuron begins releasing acetylcholine.
C) The motor neuron decreases acetylcholine release.
D) The myotube increases acetylcholine receptor expression.

Question 13

Which of the following prevent(s) outside influences from reaching the neuromuscular junction?

A) Terminal Schwann cell
B) Acetylcholine
C) Acetylcholinesterase
D) Basal lamina

Question 14

In the development of the neuromuscular junction, the function of agrin is to

A) produce neurotransmitters.
B) create Schwann cells.
C) aggregate cell membrane receptors.
D) produce the basal lamina.

Question 15

Which protein physically holds acetylcholine receptors together in place at the neuromuscular junction?

A) MuSK
B) Agrin
C) Rapsyn
D) LRP4

Question 16

Which protein promotes acetylcholine receptor expression at the neuromuscular junction?

A) Neuroligin
B) Neurexin
C) Agrin
D) Neuregulin

Question 17

Which protein promotes the maturation of Schwann cells to myelinate motor neuron axons?

A) Neuroligin
B) Neurexin
C) Agrin
D) Neuregulin

Question 18

After muscle damage, what guides regenerating motor neuron axons back to their former site at the neuromuscular junction?

A) Acetylcholine receptors on the muscle fibers
B) Basal lamina from the NMJ
C) Schwann cells
D) Acetylcholine secreted by motor neurons

Question 19

After muscle damage, muscle fibers regenerate new clusters of acetylcholine receptors at their former neuromuscular junction site even in the absence of any motor neuron innervation, and motor neurons return to their former NMJ site even if muscle fibers are prevented from regenerating. What does this suggest about NMJ development and regeneration?

A) Motor neurons are not required for the initial development of the NMJ.
B) Something in the muscle fiber marks the site of the NMJ.
C) Something in the extracellular matrix marks the site of the NMJ.
D) Something in the motor neuron marks the site of the NMJ.

Question 20

Acetylcholine receptors are an example of what type of ion channel?

A) Ligand-gated
B) Voltage-gated
C) Cotransporter
D) Diffusible

Question 21

Mature synapses distinguished from embryonic synapse by their

A) longer postsynaptic potentials.
B) shorter postsynaptic potentials.
C) release of more neurotransmitter.
D) stronger postsynaptic potentials.

Question 22

In axons, the gap between segments of myelin is called a _______, and it serves to _______ action potential conduction.

A) node of Ranvier; slow down
B) oligodendrocyte; slow down
C) node of Ranvier; speed up
D) oligodendrocyte; speed up

Question 23

Which human disorder results from the degeneration of myelin in the central nervous system?

A) Marie-Charcot-Tooth disease
B) Guillain-Barre syndrome
C) Multiple sclerosis
D) ALS

Question 24

Which human disorder results from the degeneration of myelin in the peripheral nervous system?

A) Marie-Charcot-Tooth disease
B) Guillain-Barre syndrome
C) Multiple sclerosis
D) ALS

Question 25

If the gene for Nogo was knocked out, _______ axonal regeneration would occur in the _______ nervous system.

A) no; peripheral
B) no; central
C) more; peripheral
D) more; central

Question 26

What is a possible advantage of the postsynaptic response being short-lived rather than longer-lasting?

Question 27

What is one possible reason why Fragile X syndrome is more common in males than in females?

Question 28

What experimental results indicate that the binding of neurexins and neuroligins is both necessary and sufficient to trigger the first steps of synapse formation?

Question 29

The motor neuron, muscle fiber, and Schwann cells all produce agrin. Why does the agrin produced in the muscle fiber not cause acetylcholine receptors to aggregate together before contacting the motor neuron? What would happen if only the agrin produced by motor neurons was mutated?

Question 30

How can the neuromuscular junction have large aggregations of acetylcholine receptors if electrical activity of the muscle decreases the expression, aggregation, and stabilization of AChR? What is a possible advantage to having muscle activity suppress AChR?

Question 31

Refer to the figure.
Each graph represents the depolarization activity during an action potential in Xenopus spinal cells at different stages of development. Referring to each electrical reading (A, B, and C), place the graphs in order of developmental stage, from earliest to latest. What are the major changes in action potential activity that occurs with development?

Question 32

In what way does the function of GABA receptors change across development? What mechanism mediates this change?

Question 33

Refer to the figure.
These data show the maturation of excitatory synapses in the rat neocortex. From the graph, what can you conclude about how the duration of the postsynaptic potential changes as development progresses? What does the reduction in standard deviation error bars indicate?

Question 34

What two types of glia myelinate axons, and where do you find them? What is the function of myelination?

Question 35

Why can severed axons in the periphery regenerate and reinnervate muscle, but severed axons in the brain or spinal cord rarely or never innervate their appropriate target? Why might humans have not evolved a way to regenerate CNS connections?