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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
Q

How is DA synthesized

A

phenylalanine
– Tyrosine
– DOPA
– DOPAMINE

26
Q

how is DA mainly terminated by what

A

Mainly by reuptake COMT, then Enzyme MAO

27
Q

how does DOPA effect DA

A

increases the supply of DA being produced

28
Q

how does Reserpine effect DA

A

causes leaking from vesticles, destoyed by MAO

29
Q

how does cocaine effect DA

A

blocks the retake of DA, (blocking COMT)

30
Q

how does AMPT effect DA

A

Tyrosine inhibitor , so it’s an antagonist less da is produced

31
Q

*** how does amphetamine effect DA

A

increases the release of DA

32
Q

how does imipramine effect DA

A

blocks reuptake

33
Q

how does chlorpromazine effect DA

A

(anti psychotic) blocks the dopamine recetors

34
Q

how does iproniaziad effect DA

A

Blocks MAO

35
Q

Tropolane

A

Blocks COMT (helps with reuptake)

36
Q

how does haloperidol effect DA

A

(anti psychotic) blocks the dopamine recetors

37
Q

an excess of DA in the fore brain causes

A

schizophrenia

38
Q

what area of the brain is extreme affinity to DA

A

Neucleas acumbance

39
Q

what 2 areas of the brain produce DA

A

VTA, substancia nigra

40
Q

How is NE synthesized

A

phenylalanine
– Tyrosine
– DOPA
– DOPAMINE HYDROXLASE

41
Q

how is NE mainly terminated by what

A

Mainly by reuptake COMT, then Enzyme MAO

42
Q

what are the receptor and the sub types for NE

A

adrenergic receptors, Alpha and Beta

43
Q

where is NE used in periphery

A

Sympathetic post-ganglionic

44
Q

list the effect of NE, IS, EPI in greatest to least effective alpha adrenergic receptors

A

NE, EPI, IS, (isperternol)

45
Q

list the effect of NE, IS, EPI in greatest to least effective beta adrenergic receptors

A

IS, (isperternol) EPI, NE,

46
Q

alpha adrenergic receptors antagonist, effect

A

phenoxybenzamine, lower blood presure

47
Q

beta adrenergic receptors antagonist, effect

A

propranolol, lowers blood pressure and help with uneven heart beat

48
Q

How is GABA synthesized

A

Glucose –>Glutamate, glutamine, ( glutaminese )

• Glutamate (GAD - vitamin B6) GABA

49
Q

how is GABA mainly terminated by what

A

(GABA-T)

50
Q

what are the fast receptors GABA uses , what do ultimately do

A

inotropic receptors, that open Cl- channels make the response negative

51
Q

what are the slow receptors GABA uses , what do ultimately do

A

metatropic receptors, that open K+ channel (K leaves) make the response negative

52
Q

How does alcohol effect GABA receptors

A

effects ionotropic Cl-, so it slows stuff down

53
Q

How is Gultimate synthesized

A

Glucose –>Glutamate, glutamine, ( glutaminese )

• Glutamate

54
Q

whats does the fast glutamate receptors do

A

AMPA receptors, MG2+ make the membrane more posiitive they make more AMPA,

55
Q

whats does the fast glutamate receptors do

A

NMDA memory acquisition

56
Q

AMPA receptor antagonists:

A

some new Benzodiazepines

57
Q

NMDA receptor antagonists

A

PCP, Ketamine, several opiates, alcohol

psy 311 (4 decks)

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