Structural and Functional Properties of Neurons (and Glia)

Question 1

Which class of microtubule-associated motor proteins moves stuff anterograde? Retrograde?

Answer 1

Anterograde: Kinesins.
Retrograde: Dyneins

Question 2

Why do chemotherapy drugs targeting microtubles cause neuropathy?

Answer 2

They disrupt microtubules used for axonal transport.

Question 3

CTB review: To which ions are neurons (and other cells) most permeable at rest?

Answer 3

K+

Question 4

CTB review: Why doesn’t the action potential propagate backwards down the axon?

Answer 4

Upstream Na+ channels deactivate.

Question 5

From which germ layer are microglial derived?

Answer 5

mesoderm

Question 6

Name 5 roles of glia:

Answer 6

1. Regulation of cell migration and axon guidance.
2. Formation of the BBB.
3. Trophic and insulating functions (myelination)
4. Modulation of synaptic function.
5. Mediate response to injury

Question 7

CTB review: Which cells myelinate in the CNS? How about in the PNS?

Answer 7

CNS: oligodendrocytes
PNS: Schwann cells

Question 8

What is Charcot-Marie-Tooth? What is its genetic cause?

Answer 8

Demyelination disorder caused by dominant mutations in PMP22, peripheral myelin protein 22. (Charcot aka. “The Napoleon of Neuroses” was a pimp.)

Question 9

What’s the neurotransmitter used at the neuromuscular junction?

Answer 9

Acetylcholine (ACh)

Question 10

Will depolarization of the presynaptic cell always cause the post-synaptic muscle to contract? Why or why not?

Answer 10

Yes. All NMJs are excitatory.

Question 11

Will depolarization of a pre-synaptic neuron always cause an action potential in a post-synaptic neuron of the CNS? Why or why not?

Answer 11

No. Excitatory and inhibitory signals must be integrated by the post-synaptic cell.

Question 12

How can neurotransmitters be released so quickly? (two important processes)

Answer 12

Vesicles are primed a sit on the membrane, waiting for Ca++ influx to trigger membrane fusion and neurotransmitter release (this takes only 1msec). Recycling of vesicles by endocytosis is also important.

Question 13

What are 2 ways neurotransmitters act on ion channels?

Answer 13

Directly, by binding to ligand-gated ion channels. Indirectly, but acting through at GPCR.

Question 14

Where is the “decision” to fire an AP in the muscle made?

Answer 14

At the NMJ (neuromuscular junction)

Question 15

Where is the “decision” to fire an AP in a neuron made?

Answer 15

At the axon hillock.

Question 16

What two variables does the ability to transmit and AP received from a pre-synaptic cell depend upon?

Answer 16

Time constant and length constant.

Question 17

What is the significance of having a longer time constant or longer length constant?

Answer 17

Having a either a longer time or length constant means that it takes longer for the depolarization to decay per unit time/length; and thus an AP is more likely to be generated at the axon hillock. (Longer = easier to make AP)

Question 18

Practically applying your understanding of the length constant… Given APs of equal magnitude, what is the place for the pre-synaptic terminus to contact the post-synaptic cell that is most likely to induce an AP in the post-synaptic cell: Dendrite spine, dendrite shaft, or cell body?

Answer 18

Cell body, because it’s closest to the axon hillock.

Question 19

Describe pre-synaptic inhibitition and facilitation.

Answer 19

In both cases, a second pre-synaptic neuron makes contact with the first pre-synaptic neuron on its axon. In presynaptic inhibition, the second pre-synaptic neuron sends an inhibitory signal to the first pre-synaptic neuron, making it less likely that an AP will be triggered in the post-synaptic cell. In pre-synaptic faciliation… the opposite. (see slide 30 if this is confusing) **corrected…

Question 20

What happens when a PNS axon is cut? (3 steps) What is this process called?

Answer 20

Schwann cells unwind from the axon, macrophages clear the axon debris in 1-2 days, and Schwann cells stay in place to provide the framework for an axon to be rebuilt there.
This is called Wallerian degeneration.

Question 21

How does the distribution of Nissl substance change in an injured motor neuron?

Answer 21

It goes from hanging out in the ER in the cell body… to just going away.

Question 22

How does Wallerian degeneration in the CNS differ from that in the PNS?

Answer 22

In the CNS, it takes much longer for debris to be cleared by microglia (weeks to months). Also, axonal damage can kill the proximal cell and cause degeneration of the post-synaptic cell.

Question 23

Name 3 factors that inhibit regeneration of axons in the CNS.

Answer 23

1. Inhibitory environment for growth (the glial scar)
2. Inhibitory molecules present in CNS myelin.
3. Low intrinsic growth of adult neurons

Question 24

Name 3 growth-inhibitory molecules present in CNS myelin. Has inhibiting these worked well therapeutically?

Answer 24

Nogo, MAG, and Slit. Unfortunately, no.