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psy 311 > Neurotranmitters > Flashcards

Neurotranmitters Flashcards

1
Q

What are the the criteria for neurotransmitter

A

1) present In pressman pic terminal
2) mechanism for synthesis
3) must be released when stimulated
4) mechanism for termination
5) application for an agonist and antagonist

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2
Q

How is ACh synthesized

A

Choline, coenzyme A, acetyl group

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3
Q

where is ACh used (broadly)

A

neuromuscular junction in skeletal muscles

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4
Q

how is Ach mainly terminated , by what ?

A

deactivation by Acetylcholine Esterase ( AChE ) enzyme

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5
Q

what are the receptor sub types for Ach

A

Nicotinic (ionotropic, fast) Vs Muscarinic (metabotropic, Slow)

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6
Q

Agonists: Nicotinic and Muscarinic

A

Nicotine and Muscarine

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7
Q

Antagonists: Nicotinic and Muscarinic

A

Curare and Atropine

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8
Q

Skeletal muscles at neuromuscular junction use nicotinic receptors so the agonist and Antagonists are

A

Agonist: nicotine

– Antagonist: curare

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9
Q

where is ACh used in the Autonomic Nervous System

A

Sympathetic: pre-ganglionic only,

Parasympathetic: pre and post ganglionic

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10
Q

in the Sympathetic NS what would happen if Curare was added

A

the action would be slowed down because there is no release of Ach

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11
Q

in the parasympathetic NS what would happen if Curare was added to pre ganglion

A

?

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12
Q

in the parasympathetic NS what would happen if Atropine was added to post ganglion

A

?

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13
Q

in the Brain:Tegmental Recticular Formation uses what type of receptor :

A

muscarinic

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14
Q

what is the antagonist for AChE, what happens when it is added

A

Physostigmine (ESERIN), stops AChE and more ACh is left in cleft

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15
Q

what does the Renshaw cell do in spinal cord, what type of receptor does it use

A

sends feed back to motor neurons, allows for smooth movements, used nicortinic receptors

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16
Q

How is 5-HT synthesized

A

tryptophan –>

• 5-hydroxy tryptophan Oxidase)–> 5_HT

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17
Q

how is 5-HT mainly terminated by what

A

by reuptake,Enzyme: (MAO)

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18
Q

Reserpines effect on 5-HT transmission

A

destroyes the synaptic vesticles so 5-HT will leak and MAO will depleate it , so the action will be lessen

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19
Q

LSD affect on 5-HT

A

LSD occupies the 5-HT receptors, so the body will make more receptors, wehn LSD is gone there is a higher effect of 5-HT because it binds to more receptors

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20
Q

Prozac effect on 5-HT

A

antagonist, blocks the reuptake of 5-HT

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21
Q

Iproniazid effect on 5-HT

A

agonist, that is a anti depressent that inhibits MAO

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22
Q

what Serotonin as transmitter: In the periphery:

A

smooth muscles in (gut)

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23
Q

what are the receptor sub types for 5-HT

A

ionotropic, metabatropic

24
Q

what happens In brain when something messes with 5-HT

A

: AH (shivering), RF slow wave sleep (PCPA) In brain: Limbic System (mood), cortex (hallucinations)

25
How is DA synthesized
phenylalanine – Tyrosine – DOPA – DOPAMINE
26
how is DA mainly terminated by what
Mainly by reuptake COMT, then Enzyme MAO
27
how does DOPA effect DA
increases the supply of DA being produced
28
how does Reserpine effect DA
causes leaking from vesticles, destoyed by MAO
29
how does cocaine effect DA
blocks the retake of DA, (blocking COMT)
30
how does AMPT effect DA
Tyrosine inhibitor , so it's an antagonist less da is produced
31
*** how does amphetamine effect DA
increases the release of DA
32
how does imipramine effect DA
blocks reuptake
33
how does chlorpromazine effect DA
(anti psychotic) blocks the dopamine recetors
34
how does iproniaziad effect DA
Blocks MAO
35
Tropolane
Blocks COMT (helps with reuptake)
36
how does haloperidol effect DA
(anti psychotic) blocks the dopamine recetors
37
an excess of DA in the fore brain causes
schizophrenia
38
what area of the brain is extreme affinity to DA
Neucleas acumbance
39
what 2 areas of the brain produce DA
VTA, substancia nigra
40
How is NE synthesized
phenylalanine – Tyrosine – DOPA – DOPAMINE HYDROXLASE
41
how is NE mainly terminated by what
Mainly by reuptake COMT, then Enzyme MAO
42
what are the receptor and the sub types for NE
adrenergic receptors, Alpha and Beta
43
where is NE used in periphery
Sympathetic post-ganglionic
44
list the effect of NE, IS, EPI in greatest to least effective alpha adrenergic receptors
NE, EPI, IS, (isperternol)
45
list the effect of NE, IS, EPI in greatest to least effective beta adrenergic receptors
IS, (isperternol) EPI, NE,
46
alpha adrenergic receptors antagonist, effect
phenoxybenzamine, lower blood presure
47
beta adrenergic receptors antagonist, effect
propranolol, lowers blood pressure and help with uneven heart beat
48
How is GABA synthesized
Glucose -->Glutamate, glutamine, ( glutaminese ) | • Glutamate (GAD - vitamin B6) GABA
49
how is GABA mainly terminated by what
(GABA-T)
50
what are the fast receptors GABA uses , what do ultimately do
inotropic receptors, that open Cl- channels make the response negative
51
what are the slow receptors GABA uses , what do ultimately do
metatropic receptors, that open K+ channel (K leaves) make the response negative
52
How does alcohol effect GABA receptors
effects ionotropic Cl-, so it slows stuff down
53
How is Gultimate synthesized
Glucose -->Glutamate, glutamine, ( glutaminese ) | • Glutamate
54
whats does the fast glutamate receptors do
AMPA receptors, MG2+ make the membrane more posiitive they make more AMPA,
55
whats does the fast glutamate receptors do
NMDA memory acquisition
56
AMPA receptor antagonists:
some new Benzodiazepines
57
NMDA receptor antagonists
PCP, Ketamine, several opiates, alcohol

psy 311 (4 decks)

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