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Med School > CTCS Quiz 3 > Flashcards

CTCS Quiz 3 Flashcards

1
Q

What is the distance between pre and post-neuromuscular junction membranes? Is this enough to prevent a flow of current?

A

20nm. Yes.

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2
Q

What type of message is used in the neuromuscular junction?

A

A chemical message.

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3
Q

What sort of gates are located on the presynaptic membrane?

A

Voltage gated Ca++.

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4
Q

What sort of synapse uses ACh (acetylcholine)?

A

Cholinergic.

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5
Q

What is the axon hillock?

A

The hillock is the place on the nerve that decides whether or not to send the AP.

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6
Q

What is the effect of APs traveling back up the neuron?

A

It can affect plasticity.

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7
Q

What is an axosomatic synapse?

A

A synapse on the body of a nerve cell.

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8
Q

What is an axodendritic synapse? How many types?

A

A synapse on the dendrite of a cell. Two types: 1) spine and 2) shaft.

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9
Q

What is an axo-axonic synapse?

A

When the synapse is right on the bouton.

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10
Q

What is a quantal content? What is the average in the NMJ as compared to CNS?

A

of quanta released per AP. NMJ avg. 40-80. CNS is much lower.

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11
Q

What is post-tetanic potentiation/depression?

A

Several seconds after many, rapid APs are fired, you fire another one and the AP can be increased (potentiation) or reduced (depression).

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12
Q

What is low-frequency depression?

A

Slow, repetitive action in a pathway that results in an AP of diminishing magnitude. Habituation.

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13
Q

What is a retrograde chemical messenger?

A

A post-synpase releases a messenger that increases the production of the pre-synaptic neuron. This could be nitric oxide.

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14
Q

What is homologous desensitization for a GCPR?

A

GPCR kinase (GRK) phosphorylates GPCR, this recruits arrestin, GPCR is endocytosed and either degraded or recycled.

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15
Q

What is heterologous desensitization for a GPCR?

A

Repeated stimulation that leads to a desensitivity.

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16
Q

What does a competitive antagonist do to Vmax and Km?

A

Vmax is the same.

Km is increased.

17
Q

What does a noncompetitive antagonist do to Vmax and Km?

A

Vmax is decreased. Km is the same.

18
Q

What is an agonist, antagonist and inverse agonist?

A

Agonist: response
Antagonist: no response
Inverse Agonist: decreased response

19
Q

What does Ga-S do?

A

activates cAMP

20
Q

What does Ga-i do?

A

inhibits cAMP

21
Q

What does Ga-q do?

A

activates PLC-beta which increases DAG (activates PKC) and IP3 (increases intracellular Ca++)

22
Q

How does Gs regulate adenylyl cyclase?

A

Gs activates adenylyl cyclase which coverts ATP to cAMP which then activates PKA.

23
Q

How does rhodopsin work with a Ca++ receptor?

A

Rhodopsin has a Gprotein, it activates cGMP/PDE which makes cGMP and keeps the Ca++ channel open. This is darkness. The channel closes when there is light.

24
Q

What does DAG activate?

A

PKC

25
Q

What does IP3 activate?

A

Ca++ channels. It increase intracellular Ca.

26
Q

How does Gq affect DAG and IP3?

A

Gq activates PLC-b, converts PIP2 to DAG and IP3.

27
Q

How can a GPCR regulate cell growth, motility and proliferation?

A

GPCR activates PI-3K which activates TFs associated with cell growth, proliferation and motility.

28
Q

What is transautophosphorylation?

A

When RTK dimerizes they becomes active and cross-phosphorylate each other.

29
Q

What is a GEF?

A

Guanine Exchange Factor. Turns GDP into GTP and helps to activate RAS G protein.

30
Q

What is GAP?

A

GTPase Activating Protein. Helps RAS G proteins to turn GTP to GDP, thus inactivating the protein.

31
Q

What is RAS?

A

RAS is a small G protein. GEF helps to activate it and GAP helps to deactivate it. It is a monomeric protein.

32
Q

How does RTK make IP3?

A

RTK binds to SH2 which recruited PLC gamma. That turns PIP2 into DAG and IP3.

33
Q

What is the fxn of IP3?

A

IP3 opens channels to increase intracellular Ca++ levels.

34
Q

What is the primary excitatory transmitter in the CNS? Primary inhibitory?

A

Excite: Glutamate

Inhibit: Gaba, Glycine

35
Q

How many keys does the NMDA need to be opened? What are they?

A
  1. A voltage-gated channel and a glutamate gate.
36
Q

What are two ways to activate PI-3K?

A

RTK and beta/gamma subunits.

Med School (24 decks)

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