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Medical Neuroscience > Lectures 17 & 18 Neurotransmitters and Neuromodulators > Flashcards

Lectures 17 & 18 Neurotransmitters and Neuromodulators Flashcards

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USMLE® Step 1 flashcards
1
Q

What type of receptor are cholinergic N1 and N2 receptors?

A

ionotropic

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2
Q

What is PDE? What is its action?

A

PDE- Phosphodiesterase

it breaks down cAMP into 5’ AMP

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3
Q

What effector protein is activated by G-S?

A

Adenylyl cyclase (AC)

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4
Q

What does Adenylyl cyclase do?

A

AC produces cAMP from ATP

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5
Q

What enzyme can produce cAMP from ATP?

A

Adenylyl cyclase

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6
Q

How is cAMP action terminated?

A

breakdown by phosphodiesterase (PDE)

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7
Q

What are 2 ways that the concentration of cAMP can be regulated?

A
  1. rate of synthesis by adenylyl cyclase (AC)

2. breakdown by phosphodiesteras (PDE)

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8
Q

What does cAMP do? How is it made?

A

cAMP can activate and ion channel or another protein

It is made by adenylyl cyclase from ATP (AC is activated by a G-S protein)

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9
Q

What happens to a g protein when GDP is exchanged for GTP?

A

it becomes activated

alpha subunit dissociates from beta-gamma subunit and they both go to interact with efferectors

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10
Q

How are G-proteins inactivated?

A

the alpha sub-unit hydrolyzes the GTP back to GDP and the alpha, beta and gamma units again form a trimer (inactive)

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11
Q

How does caffeine affect phosphodiesterase (PDE)?

A

decreases PDE thus increasing effects of cAMP

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12
Q

How does G-C work?

A

activates guanylate cyclase to generate cGMP (similar to G-s that generates cAMP)

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13
Q

How does G-i work?

A

decreases adenylyl cyclase activity and thus decreases cAMP production–>inhibition/modulation of ion channels (alpha-2 autoreceptors work in this manner-NE)

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14
Q

What do G-q proteins activate?

A

phospholipase C (PLC)

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15
Q

What 2 second messengers are produced as a result of PLC activation by Gq?

A

IP3 and DAG

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16
Q

What does IP3 do?

A

causes release of calcium from the endoplasmic reticulum

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17
Q

What does DAG do?

A

activates PKC

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18
Q

What are the 3 second messengers produced as a result of Gq mediated activation of PLC?

A

IP3
DAG
Ca

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19
Q

How does G-olf work?

A

causes an increase in cAMP which increases Na permeability–> depolarization of olfactory neurons

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20
Q

What system is G-t found in? Is is inhibitory or excitatory?

A

transducin in the retina-visual system

inhibitory

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21
Q

List the 6 g-protein cascades we discussed.

A 
G-S
G-C
G-Q
G-OLF
G-T
G-i
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22
Q

Of the 6 g-protein cascades we discussed which two decrease the amount of cAMP (inhibitory?)

A

G-t

G-i

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23
Q

Of the 6 G-protein cascades we discussed, which two increase the amount of cAMP?

A

G-s

G-olf

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24
Q

Which g-protein cascade releases internal calcium stores using IP3 as a 2nd messenger?

A

Gq

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25
Q

Which g-protein cascade increases production of cGMP?

A

G-c

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26
Q

What are the two major classes of Cholinergic receptors?

A

Nicotinic (2 subtypes)

Muscarinic (5 subtypes)

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27
Q

Where are N-1 receptors found?

A

skeletal muscle

28
Q

Where are N-2 receptors found?

A

ANS

29
Q

Are cholinergic muscarinic receptors excitatory or inhibitory?

A

depends on location

  • GI Tract- excitatory (M1)
  • Heart-inhibitory (M2)
30
Q

What blocks the M1 receptor?

A

atropine

31
Q

What type of g-protein is the M1 receptor in the GI tract?

A

Gq- uses IP3 messanger system to increase gCa and cause depolarization–>excitation

32
Q

Are the nicotinic ACh-R ionotropic or metabotropic?

A

ionotropic

33
Q

Are the muscarinic ACh-R ionotropic or metabotropic?

A

metabotropic

34
Q

What can a lack of Norepinephrine cause?

A

depression

35
Q

How do tricyclics work?

A

by blocking NE re-uptake–> elevate mood

36
Q

How do MAO-Is work to treat depression?

A

inhibit monoamine oxidase (which breaks down NE) and thus increase NE in terminal

37
Q

Are dopamine receptors ionotropic or metabotropic?

A

all metabotropic

38
Q

What are the three catecolamines?

A

dopamine, epinephrine and norepinephrine (DA, E and NE)

39
Q

What neurotransmitter is involved in parkinson’s disease?

A

dopamine decreased (death of cells in substantia nigra)

40
Q

How are D-1 and D-2 receptors different?

A

D-1 receptors are excitatory and cause and increase in cAMP (through Gs)

D-2 receptors are inhibitory and cause a decrease in cAMP (through Gi)

41
Q

How many metabotropic GPCRs for dopamine have been identified?

A

4

42
Q

Which condition is marked by high numbers of D-4 dopamine receptors?

A

Schizophrenia (treated with phenthiazines like thorazine-block D-4 receptors- DA antagonist)

43
Q

How is dopamine cleared from the synaptic cleft?

A

Na-coupled transporter (blocked by cocaine and amphetamines)

44
Q

What is serotonin (5-HT) synthesized from?

A

tryptophan

45
Q

How many 5-HT receptors have been identified?

A

16 (15 GPCRS, 1 Ionotropic)

46
Q

What two illegal drugs cause a transient increase in 5-HT?

A

LSD and ectasy

47
Q

What does histamine control?

A

wakefulness, arousal

48
Q

What are the 2 main excitatory amino acid NTs in the brain?

A

glutamate and aspartate

49
Q

What are the 2 main inhibitory amino acid NTs in the brain?

A

GABA and Glycine

50
Q

What are the two opoid peptides?

A

endorphin and enkephalin

51
Q

What are the 2 ionotropic receptors for glutamate?

A

NMDA, AMPA, kainate

52
Q

Why is the gating of the glutamatergic NMDA receptor unusual?

A

it is both ligand and voltage gated (Mg stuck in channel-removed above -60mV)

53
Q

What is the major inhibitory NT in the brain?

A

GABA

54
Q

What are the two type of GABA receptors?

A

GABA-A and GABA-B

55
Q

How do GABA-A receptors function?

A

ionotropic receptor that increases gCl which opposes depolarization and results in inhibition

56
Q

How do GABA-B receptors function?

A

metabotropic receptors that act through the Gi mechanism to decrease cAMP, gCa and cause inhibition

57
Q

How do barbiturates and benzodiazepines such as valium work?

A

enhancing the effects of GABA on gCl

ie. enhanced inhibitiion

58
Q

How does glycine work?

A

increases gCl–>inhibitory–> mostly works in the spinal cord

59
Q

What is familial startle disease caused by?

A

mutated glycine receptor

60
Q

What does strychnine block?

A

glycine channels- sometimes used by professional athletes to boost performance

61
Q

What is vasopressin aka?

A

anti diuretic hormone

62
Q

What is substance P most commonly involved in?

A

pain responsivity though recently implicated in some case of depression

63
Q

What are the gas nts?

A

NO and CO

64
Q

What does NO cause?

A

vasodilation of vascular smooth muscle (G-c pathway)

65
Q

What do NO and CO activate?

A

guanylate cyclase- Gc pathway

66
Q

How do ATP and adenosine act as NTs?

A

inhibitory NTs in the ANS

67
Q

What does viagra inhibit?

A

PDE- Phosphodiesterase- which breaks down cAMP and cGMP

Medical Neuroscience (32 decks)

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