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!!!!! Pharm spring 16 Exam 1 !!!!! > Receptors > Flashcards

Receptors Flashcards

1
Q

receptors required for action potential

A

ligand gated and voltage gated ion channels

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2
Q

Neuronal action potentials, after ACh binds to ligand gated ion channel what happens next?

A

Voltage gated Na+ channel opens THEN a voltage gated Cl-channel opens

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3
Q

an action potential starts with a _________ gated ion channel

A

Ligand gated ion channels

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4
Q

leads to action potential, positive ions go into the cell

A

Excitatory

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5
Q

Hyperpolarization, negative ions into the cells

A

Inhibitory

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6
Q

ligand binds to a receptor and activates it

A

agonist

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7
Q

ligand binds to receptor and prevents it from activating

A

antagonist

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8
Q

antagonist that acts on the main binding site

A

orthosteric antagonist

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9
Q

antagonist that acts on an accessory binding site

A

allosteric antagonist

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10
Q

antagonist that physically obstructs ion channel

A

pore blocker

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11
Q

pentamer

A

cys-loop receptors

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12
Q

tetramer

A

ionotropic glutamate receptors

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13
Q

cys-loop receptors

A

nicotinic ACh receptors
glycine receptors
5HT-3 Receptors (serotonin)
GABA-A receptors

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14
Q

ionotropic glutamate receptors

A

NMDA receptors
Kianate receptors
AMPA receptors

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15
Q

inhibitory cys-loop receptors

A

Glycine

GABA- A

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16
Q

excitatory cys-loop receptors

A

Nicotinic ACh Receptors

5HT-3 (Serotonin) Receptors

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17
Q

named fro the loop made by a disulfide bond

A

cys-loop receptors

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18
Q

physical gate of cys-loop receptors

A

the second transmembrane domain of the ALPHA subunit

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19
Q

causes ALPHA subunit to change conformation

A

agonist binding

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20
Q

drugs that act on nAChR

A

Nicotine

Varenicline (Chantix)

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21
Q

drugs that act on GABA-a

A

Ambien (Zolpidem), Barbituates, Benzodiazepines, Alcohol

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22
Q

T/F drugs have distinct binding sites that allow it to effect receptors in a unique way

A

True

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23
Q

drugs that act on NMDA receptors

A

Ketamine

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24
Q

drugs that act on AMPA receptors

A

Aniracetam (cognition enhancer)

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25
Q

nAChR subunits at neuromuscular junction

A

alpha, beta, gamma, delta

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26
Q

subunits at neuronal nAChR

A

alpha and beta

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27
Q

Receptor that pass Na, K, Ca
Has non-selective cation channels
composed of five subunits
ion passage depends on subunits

A

nAChR

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28
Q

drug that causes an UPREGULATION of receptors in response to chronic presence of drug

A

Nicotine - this is why it is hard to quit smoking

29
Q

ACh binds to _________ subunit

A

ALPHA

30
Q

not passing ion but ligand is bound

A

receptor in desensitized state

31
Q

receptor cannot be activated because a ligand is bound

A

receptor in desensitized state

32
Q

state of receptor when no ligand is bound

A

closed

33
Q

when ligand is bound and ions are actively passing receptor is

A

open

34
Q

two things that effect the propensity of a receptor to fall into a desensitized state

A
  1. what agonist is bound to the receptor

2. the subunit composition of the receptor

35
Q

AMPA, Kainate, NMDA

A

Ionotropic glutamate receptors

36
Q

only inotropic glutamate receptor that can pass calcium

A

NMDA

37
Q

the 2nd transmembrane domain forms the ion pore

A

ionotropic glutamate receptors

38
Q

each subunit has a binding site, but they are not all for glutamate

A

ionotropic glutamate receptors

39
Q

ALL 4 binding sites of these receptors MUST be occupied for the channel to open

A

ionotropic glutamate receptors

40
Q

what needs to be bound for NMDA receptors to open?

A

2 Glutamate, 2 Glycicne

41
Q

What needs to be bound for AMPA receptors to open?

A

4 Glutamates

42
Q

Gage at which cell can understand how often it is working

A

NMDA receptor activity

43
Q

_________ receptors are blocked by a _________ ion. This block is _________ dependent.

A

NMDA
Mg++
voltage

44
Q

in long term potentiation how does the NMDA receptor open?

A

Depolarization of the neuron relieves the Mg+ block and the receptor can open to pass ions

45
Q

in long term potentiation after the NMDA receptor opens what ions are passed?

A

Ca++ and Na++ come into the cell

46
Q

What specifically leads to more AMPA receptors being inserted onto the synapse?

A

NMDA receptors pass calcium which ACTIVATES Ca MKII (calcium calmodulin kinase II)

47
Q

in long term potentiation there is also a __________ messenger that goes back to the __________ terminal

A

Retrograde, pre-synaptic

48
Q

what does having more AMPA receptors on the surface mean?

A

It is a stronger synapse

49
Q

What signals to the intercellular AMPA receptors to be inserted onto the pre-synaptic terminal?

A

Calcium Calmodulin Kinase II

50
Q

Coincidence Receptors

A

NMDA Receptors

51
Q

In long term potentiation first the _______ receptors are activated which then depolarize the neuron and causes the _______ to be relieved and activate the _________ receptors which then allow a __________ influx activating ___________ to signal to the neuron to insert __________ receptors on the surface of the neuron.

A 
AMPA 
Magnesium Pore Blocker
NMDA
Ca++ and Na+
Calcium calmodulin kinase II
AMPA
52
Q

GPCR Class A

A

Adrenergic receptors

Muscarininc ACh receptors

53
Q

GPCR class B

A

Parathyroid hormone receptor

54
Q

GPCR class C

A

Metabatropic Glutamate receptors

GABA-b Receptors

55
Q

Excitatory
Activate Adenylyl Cyclase
increase cAMP

A

G alpa sub S Receptors

56
Q

Inhibitory
Inhibit Adenylyl Cyclase
Decrease cAMP

A

G alpha sub I Receptors

57
Q

Excitatory
Activates Phospholipase C
Increase in IP3
Release on Ca++ from intracellular stores

A

G alpha sub Q Receptors

58
Q

What is a primary factor in GPCR Desensitization?

A

B-Arrestin

59
Q

what causes B-arrestin to bind to the receptor?

A

A ligand bound to the GPCR for a prolonged period of time

60
Q

When B-arrestin binds it…

A

Tags the GPCR for internalization

61
Q

An internalized GPCR by B-Arrestin contributes to…

A

Drug tolerance

62
Q

The GPCR-B-Arrestin complex is brought inside the cell via an _________.

A

Endosome

63
Q

Three things that an endosome can do with the GPCR-B-Arrestin complex

A
  1. Degrade the complex
  2. cause an activation of signaling cascades from inside the cell that are INDEPENDENT of G Protein signaling
  3. Return the complex to the cell surface
64
Q

Time it take for B-arrestin to bind to GPCR

A

Seconds to minutes

65
Q

Time it takes B-Arrestin to internalize a GPCR

A

Minutes

66
Q

What is GRK? What does it do?

A

GPCR Kinase.

It adds a phosphate to the G-protein inside the cytoplasm.

This phosphate is what attracts B-Arrestin

67
Q

What to drugs that target the GRK (G protein coupled receptor kinase) do?

A

They can optimize agonist binding

68
Q

What is the main reason for the downstream effects of the cholera toxin?

A

Cholera toxin does not allow GTP to become a GDP resulting in A GPCR that is permanently on

69
Q

What is the GPCR that is permanently on when the cholera toxin is present and what are the downstream effects?

A

G alpha S - causes cAMP to increase dramatically.

This activates Cl- pumps which then release more Cl- into the intestinal lumen

Na+, K+ and HCO3- ions follow

H2O follows the ions to balance the osmolarity

Increased H20 in lumen = really bad diarrhea!

!!!!! Pharm spring 16 Exam 1 !!!!! (4 decks)

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