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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
inotropic GABA Rs
ligand gated ClChs GABAa R activation hyperpolarizes cell d/t influx of Cl over 15 subtypes
26
metabotropic GABA Rs
postsynaptic- increases K conductance | presynaptic- decreases Ca conductance
27
what drugs will bind GABA Rs
Benzodiazepines | barbiturates
28
glycine
ligand-gated ClChs tetanus toxin inhibits glycine release anatgonists is strychnine can act as co-agonist w/glutamate at NMDA Rs
29
Ach synthesis
in presynaptic terminal from choline and acetly-CoA via choline acetyltransferase
30
Ach Storage
Ach loaded into vesicles by VAT
31
Ach inactivation
enzymatic degradation via AchE
32
Ach ionotropic/nicotinic Rs
increases cation conductance located at NM jxn, postganglionic nn, CNS agonist- nicotine antagonist- curare-like drugs
33
metabotropic/muscarinic Ach Rs
M1- excitatory -> decreases K conductance -> increased IP3 and DAG M2- inhibitory -> increases K conductance -> decreases cAMP agonists- muscarine, pilocarpine antagonists- atropine, glycopyyrolate
34
DA synthesis
presynaptic terminal from tyrosine by enzymes tyrosine hydroxylase and dopa decarboxylase
35
DA storage
loaded into vesicles by VMAT
36
DA inactivation
reuptake mediated by high affinity DAT and low affinity PMAT
37
DA Rs
D1-5 D1- stimulatory increases cAMP D2- inhibitory: - postsynaptic -> increases K -> decreased cAMP - presynaptic -> decreases Ca conductance
38
cocaine
produces DA uptake block
39
amphetamine
increases DA release
40
NE synthesis
inside NE granules from DA via dopamine beta-hydroxylase
41
NE storage
in granules which it was produced
42
NE inactivation
reuptake into presynaptic cell mediated by NET
43
NE Rs
all metabotropic alpha 1, 2 Beta 1,2,3
44
alpha 1
excitatory decreased K conductance -> increased IP3 and DAG agonists- phenylephrine antagonists- phentolamine, prasozin
45
alpha 2
``` inhibitory postsynaptic- increases K conducatance -> decreases cAMP presynaptic -> decreases Ca conductance agonist- clonidine antagonist- yohimbine ```
46
Beta 1
excitatory decreased K conductance -> increased cAMP agonist- isoproternol antagonist- propanolol
47
beta 2
inhibitory increases cAMP agonist- albuterol antagonist- butoamine
48
5-HT synthesis
in presynaptic terminal from tryptophan via tryptophan hydroxylase
49
5-HT storage
loaded into vesicles
50
5-HT inactivation
SERT (inhibited by many anti-depressants) | pumps 5-HT back into nn terminal
51
5-HT ionotropic Rs
5-HT3 | nonselective cation Ch
52
5-HT metabotropic Rs
5HT1,2,4-7
53
5HT1
inhibitory
54
5-HT2a and 4
excitatory
55
what drugs interact with 5-HT Rs
ecstacy (MDMA) LSD ondansetron (antiemetic atypical antipychotics
56
H Rs
all are metabotropic H1-4 1 and 2 excitatory
57
peptide NT synthesisis
in cell body
58
peptide NT storage
packed into large dense core vesicles for transport down axon
59
peptide NT inactivation
unknown
60
peptide NT Rs
each peptide has its own R, usually metabotropic
61
endocannabinoids synthesis
endogenous lipophilic cannabinoids (anandamide and 2-arachidonylglycerol) occurs locally and rapidly in response to depolarization and Ca influx
62
endocannabinoids storage
non-classical NT not stored in vesicles
63
endocannabinoids release
non-classical | retrograde messengers
64
endocannabinoids Rs
all metabotropic CB1-brain inhibitory

Neuro II (22 decks)

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