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ksucpm neuro > NTS > Flashcards

NTS Flashcards

1
Q

this hypothesis states that all axon terminals of a single neuron use one and only one NT though co release of multiple transmitters has been documented?

A

Dales Hypothesis

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2
Q

the first transmitters of the PNS to be discovered?

A

Ach and Norepi

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3
Q

what is the general approach of NT release? T/F can be manipulated pharmacologically

A 
synthesis
storage
release
presynaptic receptor
high affinity reuptake
postsynaptic receptor
transmitter metabolism
postsynaptic response
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4
Q

ACh is synthesized by what enzyme? via what substrates

A

choline acetyltransferase (ChAT)

AcCoA + Choline

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5
Q

where does the AcCoA come from? choline?

A

mitochondrial metabolism of pyruvate

diet and 50% of ACh production uses recycled choline following high affinity reuptake

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6
Q

what terminates cholinergic transmission by degrading ACh to choline and acetate? where are these localized

A

choline esterase like acetylcholine esterase and made in the liver.

ACh synapses

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7
Q

name the agent based on this effect:

ACh depletion

A

-Napthylvinyl pyridine

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8
Q

name the agent based on this effect:

release vesicles, depleting number for future use

A

+B-Bungarotoxin

+Black widow spider venom (BWSV)

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9
Q

name the agent based on this effect:

few vesicles released

A

-Botulinum toxin

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10
Q

name the agent based on this effect:

deplete ACh because choline is scarce

A

-Hemicholinium

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11
Q

name the agent based on this effect:

prolongs ACh transmission, over stimulation

2 agents that are reversible and irreversible

A

-reversibly
Neostigmine
physostigmine
(medically useful)

-irreversibly
Malathion
Nerve gas
(deadly but also useful)
myasthenia gravis
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12
Q

what are is the purpose of nicotinic and muscurinic receptors and their subtypes?

A

they are found in different tissues and this allows fro more specific drugs with fewer side affects

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13
Q

dopamine-DA, norepinephrine-NE, epinphrine-EPi

A

catecholamines

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14
Q

what are the stages for the synthesis of catecholamines?

A 
L-tyrosine
L-Dopa
Dopamine
Norepinephrine
Epinephrine
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15
Q

what converts L-Tyrosine to L-Dopa?

A

tyrosine hydroxylase (cytosolic)

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16
Q

what converts L-Dopa to dopamine?

A

dopa decarboxylase (in many tissues)

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17
Q

what converts dopamine to norepinephrine?

A

dopamine-B-hydroxylase (inside many vesicles of cells that release NE)

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18
Q

what converts norepinephrine to epinephrine?

A

phenylethanolamine-N-methyl-transferase (PNMT) (cytosolic)

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19
Q

what it tyrosine hydroxylase inhibited by?

A

alpha methyl tyrosine

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20
Q

what is Dopa decarboxylase inhibited by?

A

alpha methyl dopa

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21
Q

what is dopamine-B-hydroxylase inhibited by?

A

diethyldithiocarbamate

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22
Q

what is phenylethanolamine-N-methyl-transferase stimulated by?

A

corticosteroids

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23
Q

where is epinephrine mainly found?

A

adrenal medulla and brainstem

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24
Q

what causes the release of NTs?

A

elevated intracellular Ca++

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25
Q

what agent depletes the transmitters?

A

alpha methyl tyrosine
alpha methyl dopa
diethyldithiocarbamate

26
Q

what agent displaces NT from vesicles, causing initial release but long term depletion? for DA

A

amphetamines

alpha-OH-butyrate for DA

27
Q

this is a stress hormone that enhances epi synthesis in the adrenal medulla?

A

cortisol

28
Q

this increase NE in the cleft and leads to long term NE depletion?

A

cocaine

29
Q

this enhances NE in the cleft?

A

desipramine and other tricyclic antidepressants

30
Q

this is a toxic compound taken up and destroys the terminal? this is used to produced Parkinsonism in animals

A

6-OH-dopamine

31
Q

this leads to long-lasting NE depletion in vesicles

A

reserpine

32
Q

what enzymes are used to produce VMA(NE and EPI) and HVA (DA)? found in the urine

A

monoamine oxidase

catechol-o-methyl transferase

33
Q

catechol-o-methyl transferase (COMT) inhibitor?

A

tropolone

34
Q

what is the effect of MAO inhibitors?

A

it increases the DA, NE, EPI in nerve terminals and allows for more incorporation into vesicles so more NE enters the vesicles and more NE is released

35
Q

what are MAOI’s used for?

A

antidepressants and blood pressure regulators

36
Q

where are the cell bodies of the noradrenergic neurons found?

A

locus coeruleus of the 4th ventricle

37
Q

where are the dopaminergic cell bodies found?

axons

tract

A

substantia nigra of the midbrain and most axons go to the corpus striatum (caudate and putamen) via the niagrostriatal tract

38
Q

what causes degeneration of the niagrostriatal tract?

A

MPTP

39
Q

what is MPTP an analog of what drug?

A

meperdine

40
Q

some DA neurons projet to the forebrain, what drugs specifically target synapses by blocking transmission?

A

antipsychotic drugs like haloperidol or chlorpromazine

41
Q

what is the other name for 5-hydroxytryptamine or 5-HT?

A

serotonin

42
Q

where is serotonin synthesized from?

A

L-tryptophan

43
Q

what ceases the serotonin transmission?

A

Na+ dependent high affinity reuptake by axon terminals and glia

44
Q

what are the serotonin inhibitors? what is the effect

A

clomipramine
imipramine (prozac)
fluoxetine (Zoloft)
trazodone

tranylcypromise

act to enhance serotonergic transmission and have been used in treating depression, OCD and others

45
Q

what is sertonin transmission involved in?

A

eating, sleep, sexual behavior, circadian rhythmicity, neuroendocrine function and affect

46
Q

how many classes of serotonin receptors are there?

what are the effects

A

4 major classes 5 HTI-5 HT4

increase or decrease cAMP
increase or decrease K+ permeability
stimulate ligand gated ionophore

47
Q

what is the primary excitatory NT of the CNS?

A

glutamate

48
Q

what has glutamate been implicated in?

A

epilepsy, brain damage and learning

49
Q

what terminates the glutamate transmission?

A

Na+ dependent high affinity reuptake by the neurons and glia

50
Q

what are the 4 classes of glutamate receptors? which ones are ionotropic and metabotropic?

A

NMDA
AMPA
Kainate
ionotropic

ACPD (increase Ca2+)
AP4 (decrease cAMP, cGMP)
metabotropic

51
Q

what are the inhibitory NTs?

A

GABA and glycine

52
Q

this is the main inhibitory NT of the brain, GABA released by what?

lowered gabaergic transmission is implicated in?

A

GABA

interneurons

Huntington’s disease, epilepsy, tardive dyskinesia, alcoholism, schizophrenia, and sleep disorder

53
Q

what is GABA synthesized from?

A

glutamate by glutamic acid decarboxylase

54
Q

what are the GABA receptor types? name the agonists and antagonist?

A

GABA A and B

GABA A best characterized
+isoguvacine
-bicuculline

GABA B involved in presynaptic inhibition
+baclofen
-phaclofen

55
Q

what do the GABA A receptors have binding sites for?

A

barbiturates and benediazepine

56
Q

what stimulates the benediazepine site?

A

diazepam

57
Q

what stimulates the barbiturate site?

A

phenobarnitol
pentobarbitol
Cl- channel

58
Q

what stimulates and inhibits the GABA site?

A

muscimol (hallucinogenic mushroom) stimulates

bicuculline (a convulsant)

59
Q

what enhances the Cl- conductance at the channel and depresses?

A

ETOH

Benzos and Barbs

60
Q

what is the principal inhibitor of the spine?

A

glycine, this opens the Cl- channel to produce IPSP and is inactivated by reuptake causing skeletal muscle to not contract

61
Q

what are the glycine agonist and antagonist?

A

agonist:
other amino acids not GABA

antagonist:
strychnine (muscles contract)

ksucpm neuro (54 decks)

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