CTCS Quiz 3 Flashcards

(36 cards)

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?

25
What does IP3 activate?
Ca++ channels. It increase intracellular Ca.
26
How does Gq affect DAG and IP3?
Gq activates PLC-b, converts PIP2 to DAG and IP3.
27
How can a GPCR regulate cell growth, motility and proliferation?
GPCR activates PI-3K which activates TFs associated with cell growth, proliferation and motility.
28
What is transautophosphorylation?
When RTK dimerizes they becomes active and cross-phosphorylate each other.
29
What is a GEF?
Guanine Exchange Factor. Turns GDP into GTP and helps to activate RAS G protein.
30
What is GAP?
GTPase Activating Protein. Helps RAS G proteins to turn GTP to GDP, thus inactivating the protein.
31
What is RAS?
RAS is a small G protein. GEF helps to activate it and GAP helps to deactivate it. It is a monomeric protein.
32
How does RTK make IP3?
RTK binds to SH2 which recruited PLC gamma. That turns PIP2 into DAG and IP3.
33
What is the fxn of IP3?
IP3 opens channels to increase intracellular Ca++ levels.
34
What is the primary excitatory transmitter in the CNS? Primary inhibitory?
Excite: Glutamate Inhibit: Gaba, Glycine
35
How many keys does the NMDA need to be opened? What are they?
2. A voltage-gated channel and a glutamate gate.
36
What are two ways to activate PI-3K?
RTK and beta/gamma subunits.