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Neuro II > pharm > Flashcards

pharm Flashcards

1
Q

excitatory AA transmitters

A

glutamate

aspartate

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2
Q

inhibitory AA transmitters

A

GABA

glycine

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3
Q

small molecule transmitters

A

actylcholine
monoamine
histamine

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4
Q

monoamines

A

catecholamines (dopamine and NE)

serotonin (5-HT)

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5
Q

peptides

A

opioids

tachykinins

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6
Q

opioids

A

enkephalins
endorphins
dynorphins

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7
Q

tachykinins

A

substance P

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8
Q

what is the most common effect of retrograde transmission

A

modification of NT release

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9
Q

NTs that activate inotropic Rs

A 
glutamate
GABA
Acetylcholine
glycine
5-HT
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10
Q

NTs that activate metabotropic Rs

A 
glutamate
GABA
Acetylcholine
dopamine
NE
5-HT
H2
neuropeptides
endocannabinoids
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11
Q

glutamate

A

excitatory

non-essential aa that does not cross BBB

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12
Q

glutamate synthesis

A

occurs in brain form glucose

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13
Q

glutamate storage

A

taken up into synaptic vesicles by an ATP-dependent transporter

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14
Q

inactivation of glutamate

A

initially taken up by glial cells and converted into glutamine -> transported out of glial cells into glutamatergic nn cells and converted back to glutamate

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15
Q

glutamate ionotropic Rs

A

AMPA

NMDA

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16
Q

AMPA

A

mediate vast majority of excitatory transmission in brain
ligand gated Na/K Ch
GluR1-4

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17
Q

NMDA

A

ligand gated Na/K Ch which is also highly permeable to Ca
are also voltage dependent b/c they are blocked by Mg until depolarized and then allow Ca flux
-overstimulation of these during hypoxia -> apoptosis

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18
Q

PCP (angle dust) and ketamine

A

non-competitive antagonists at NMDA R

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19
Q

NMDA R subtypes

A 
NR1
NR2A
NR2B
NR2C
NR2D
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20
Q

glutamate metabotrophic Rs

A

postsynaptic- decreases K -> increases IP3 and DAG

presynaptic -> decreased Ca conductance -> decreases cAMP

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21
Q

GABA

A

inhibitory

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22
Q

GABA synthesis

A

locally from glucose, pyruvate, or other AA precursors

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23
Q

GABA storage

A

loaded into synpatic vesicles by vesicular transporter

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24
Q

GABA inactivation

A

terminated by rapid reuptake by several types of plasma membrane transporters
also taken up by glial cells

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25
Q

inotropic GABA Rs

A

ligand gated ClChs
GABAa R activation hyperpolarizes cell d/t influx of Cl
over 15 subtypes

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26
Q

metabotropic GABA Rs

A

postsynaptic- increases K conductance

presynaptic- decreases Ca conductance

27
Q

what drugs will bind GABA Rs

A

Benzodiazepines

barbiturates

28
Q

glycine

A

ligand-gated ClChs
tetanus toxin inhibits glycine release
anatgonists is strychnine
can act as co-agonist w/glutamate at NMDA Rs

29
Q

Ach synthesis

A

in presynaptic terminal from choline and acetly-CoA via choline acetyltransferase

30
Q

Ach Storage

A

Ach loaded into vesicles by VAT

31
Q

Ach inactivation

A

enzymatic degradation via AchE

32
Q

Ach ionotropic/nicotinic Rs

A

increases cation conductance
located at NM jxn, postganglionic nn, CNS
agonist- nicotine
antagonist- curare-like drugs

33
Q

metabotropic/muscarinic Ach Rs

A

M1- excitatory -> decreases K conductance -> increased IP3 and DAG
M2- inhibitory -> increases K conductance -> decreases cAMP
agonists- muscarine, pilocarpine
antagonists- atropine, glycopyyrolate

34
Q

DA synthesis

A

presynaptic terminal from tyrosine by enzymes tyrosine hydroxylase and dopa decarboxylase

35
Q

DA storage

A

loaded into vesicles by VMAT

36
Q

DA inactivation

A

reuptake mediated by high affinity DAT and low affinity PMAT

37
Q

DA Rs

A

D1-5
D1- stimulatory increases cAMP
D2- inhibitory:
- postsynaptic -> increases K -> decreased cAMP
- presynaptic -> decreases Ca conductance

38
Q

cocaine

A

produces DA uptake block

39
Q

amphetamine

A

increases DA release

40
Q

NE synthesis

A

inside NE granules from DA via dopamine beta-hydroxylase

41
Q

NE storage

A

in granules which it was produced

42
Q

NE inactivation

A

reuptake into presynaptic cell mediated by NET

43
Q

NE Rs

A

all metabotropic
alpha 1, 2
Beta 1,2,3

44
Q

alpha 1

A

excitatory
decreased K conductance -> increased IP3 and DAG
agonists- phenylephrine
antagonists- phentolamine, prasozin

45
Q

alpha 2

A 
inhibitory 
postsynaptic- increases K conducatance -> decreases cAMP
presynaptic -> decreases Ca conductance
agonist- clonidine
antagonist- yohimbine
46
Q

Beta 1

A

excitatory
decreased K conductance -> increased cAMP
agonist- isoproternol
antagonist- propanolol

47
Q

beta 2

A

inhibitory
increases cAMP
agonist- albuterol
antagonist- butoamine

48
Q

5-HT synthesis

A

in presynaptic terminal from tryptophan via tryptophan hydroxylase

49
Q

5-HT storage

A

loaded into vesicles

50
Q

5-HT inactivation

A

SERT (inhibited by many anti-depressants)

pumps 5-HT back into nn terminal

51
Q

5-HT ionotropic Rs

A

5-HT3

nonselective cation Ch

52
Q

5-HT metabotropic Rs

A

5HT1,2,4-7

53
Q

5HT1

A

inhibitory

54
Q

5-HT2a and 4

A

excitatory

55
Q

what drugs interact with 5-HT Rs

A

ecstacy (MDMA)
LSD
ondansetron (antiemetic
atypical antipychotics

56
Q

H Rs

A

all are metabotropic
H1-4
1 and 2 excitatory

57
Q

peptide NT synthesisis

A

in cell body

58
Q

peptide NT storage

A

packed into large dense core vesicles for transport down axon

59
Q

peptide NT inactivation

A

unknown

60
Q

peptide NT Rs

A

each peptide has its own R, usually metabotropic

61
Q

endocannabinoids synthesis

A

endogenous lipophilic cannabinoids (anandamide and 2-arachidonylglycerol) occurs locally and rapidly in response to depolarization and Ca influx

62
Q

endocannabinoids storage

A

non-classical NT not stored in vesicles

63
Q

endocannabinoids release

A

non-classical

retrograde messengers

64
Q

endocannabinoids Rs

A

all metabotropic
CB1-brain
inhibitory

Neuro II (22 decks)

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