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
what agent depletes the transmitters?
alpha methyl tyrosine alpha methyl dopa diethyldithiocarbamate
26
what agent displaces NT from vesicles, causing initial release but long term depletion? for DA
amphetamines alpha-OH-butyrate for DA
27
this is a stress hormone that enhances epi synthesis in the adrenal medulla?
cortisol
28
this increase NE in the cleft and leads to long term NE depletion?
cocaine
29
this enhances NE in the cleft?
desipramine and other tricyclic antidepressants
30
this is a toxic compound taken up and destroys the terminal? this is used to produced Parkinsonism in animals
6-OH-dopamine
31
this leads to long-lasting NE depletion in vesicles
reserpine
32
what enzymes are used to produce VMA(NE and EPI) and HVA (DA)? found in the urine
monoamine oxidase catechol-o-methyl transferase
33
catechol-o-methyl transferase (COMT) inhibitor?
tropolone
34
what is the effect of MAO inhibitors?
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
what are MAOI's used for?
antidepressants and blood pressure regulators
36
where are the cell bodies of the noradrenergic neurons found?
locus coeruleus of the 4th ventricle
37
where are the dopaminergic cell bodies found? axons tract
substantia nigra of the midbrain and most axons go to the corpus striatum (caudate and putamen) via the niagrostriatal tract
38
what causes degeneration of the niagrostriatal tract?
MPTP
39
what is MPTP an analog of what drug?
meperdine
40
some DA neurons projet to the forebrain, what drugs specifically target synapses by blocking transmission?
antipsychotic drugs like haloperidol or chlorpromazine
41
what is the other name for 5-hydroxytryptamine or 5-HT?
serotonin
42
where is serotonin synthesized from?
L-tryptophan
43
what ceases the serotonin transmission?
Na+ dependent high affinity reuptake by axon terminals and glia
44
what are the serotonin inhibitors? what is the effect
clomipramine imipramine (prozac) fluoxetine (Zoloft) trazodone tranylcypromise act to enhance serotonergic transmission and have been used in treating depression, OCD and others
45
what is sertonin transmission involved in?
eating, sleep, sexual behavior, circadian rhythmicity, neuroendocrine function and affect
46
how many classes of serotonin receptors are there? what are the effects
4 major classes 5 HTI-5 HT4 increase or decrease cAMP increase or decrease K+ permeability stimulate ligand gated ionophore
47
what is the primary excitatory NT of the CNS?
glutamate
48
what has glutamate been implicated in?
epilepsy, brain damage and learning
49
what terminates the glutamate transmission?
Na+ dependent high affinity reuptake by the neurons and glia
50
what are the 4 classes of glutamate receptors? which ones are ionotropic and metabotropic?
NMDA AMPA Kainate ionotropic ACPD (increase Ca2+) AP4 (decrease cAMP, cGMP) metabotropic
51
what are the inhibitory NTs?
GABA and glycine
52
this is the main inhibitory NT of the brain, GABA released by what? lowered gabaergic transmission is implicated in?
GABA interneurons Huntington's disease, epilepsy, tardive dyskinesia, alcoholism, schizophrenia, and sleep disorder
53
what is GABA synthesized from?
glutamate by glutamic acid decarboxylase
54
what are the GABA receptor types? name the agonists and antagonist?
GABA A and B GABA A best characterized +isoguvacine -bicuculline GABA B involved in presynaptic inhibition +baclofen -phaclofen
55
what do the GABA A receptors have binding sites for?
barbiturates and benediazepine
56
what stimulates the benediazepine site?
diazepam
57
what stimulates the barbiturate site?
phenobarnitol pentobarbitol Cl- channel
58
what stimulates and inhibits the GABA site?
muscimol (hallucinogenic mushroom) stimulates bicuculline (a convulsant)
59
what enhances the Cl- conductance at the channel and depresses?
ETOH Benzos and Barbs
60
what is the principal inhibitor of the spine?
glycine, this opens the Cl- channel to produce IPSP and is inactivated by reuptake causing skeletal muscle to not contract
61
what are the glycine agonist and antagonist?
agonist: other amino acids not GABA antagonist: strychnine (muscles contract)