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94 Cards in this Set
- Front
- Back
t/f
sympathetic preganglionic fibers are long |
f
short |
|
sympathetic has ----- postganglionic fibers
|
long
|
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sympathetic nerve s contain -------
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varicosity's
|
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each varicosity is a nerve ----- in which ---- can be released
|
terminal
NE |
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where do you get your tyrosine from
|
diet
|
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how is tyrosine converted to L DOPA
|
via tyrosine hydroxylase
|
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L DOPA is changed converted to dopamine via
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aromatic L amino acid decarboxylase
|
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rate limiting step of the catcholamine synthesis
|
tyrosine hydroxylase
|
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from tyrosine to L dopa what's added
|
OH
|
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from L dopa to dopamine what's removed
|
COOH
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where's is dopamine found
|
substantia nigra
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dopamine to norepi.
what's the enzyme |
dopamine B hydroxylase
|
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what's added to dopamine to become norepi
|
OH
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from norepi to epi
enzyme? |
PMNT
|
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What's added to norepi to become epi
|
CH3
|
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t/f
tyrosine is goes in the cell body due to the change concentration gradient |
f
due to active transport |
|
----- is taken up in to the vesicles to become norepi
what's contained inside the vesicles |
dopamine
dopamine B hydroxylase |
|
t/f
epi is made inside the vesicles |
f
NE comes out of the vesicles and meets PMNT, then epi is made and it goes back in the vesicle |
|
what activates the nerve impulse so the surface of the vesicle binds to the membrane
|
Ca 2+ influx
|
|
what 2 enzymes can inactive norepi
|
COMT
MAO |
|
t/f
a dopamine neuron will express dopamine B hydroxylase |
F
it will not if it's not going to be changed to norepi or epi |
|
what two neurons will express Dopamine B hydroxylase
|
norepi
epi |
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will a norpi neuron express PMNT
|
no
only an epi will |
|
t/f
the catecholamine synthesis occurs only in the neurons |
f
in both neurons and adrenal medulla |
|
what releases epi
|
adrenal medulla
|
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thru what method does DA get into the vesicle
|
active transport
|
|
t/f
once norepi is out of the cell body it can no longer be used |
f
it will go back into the vesicle, into a cell body. it will be reused. |
|
3 ways in which norepi inactivated
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1. taken back into vesicles
2. enzymatically inactivated 3. Norepi binds to the A2 receptor/autoreceptor |
|
t/f
only one enzyme is need to deactivate norpi |
f
both are needed |
|
the enzymes need to deactivate norepi
|
COMT
MAO |
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which inactivation enzyme is extracellular
how does it deactivate the norepi |
COMT
it adds replaces an OH w/ a CH3 |
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which enzyme replaces NH2 w/ a COOH
|
MAO
|
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what occurs if there's too much norepi w/in the cell body, that's not in the vesicles
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mao will deactivate, it will leave, and comt will then replace the OH w/ a CH3
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what occurs if the norepi is in the synapse and it is to be enzymatically deactivated
|
comt will replace the OH w/ a CH3, then it will be sent inside cell body to have the NH2 replaced w/ the COOH, it wil then leave the cell body and go into blood
|
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comt and mao changes deactivates by changing the -- for the receptor
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affinity
|
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what prevents metabolism by MAO or diffusion out
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storage in vesicles
|
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what do you call when the entire contents of is released
|
quantel
|
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how do you increase a response
|
increase the # of vesicles that's will release norepi, not how much will be released per vesicle. . . this can't be done anyway because of quantel release!
|
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where does uptake 1 take place
|
neuronal cells
|
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which is most responsible for reuptake uptake 1 or 2
|
uptake 1
|
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what has the greatest affinity for reuptake
EPI DA NE |
1. DA
2. NE 3. EPI |
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4 things uptake 1 is dependent on
|
1. Energy
2. Sodium 3. Temperature 4. Saturable |
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where does uptake 2 take place
|
extraneuronal cells
|
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t/f
uptake 1 is not saturable |
f
saturable |
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which uptake deals w/ nonspecfic binding
|
uptake 2
|
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name the transporter in uptake 2
|
OCT-1
OCT-2 OCT-3 |
|
t/f
in oct1 the affinity of DA and EPI and NE are the same |
f
DA and EPI are the same, but NE is less |
|
the affiniity of oct-2 for epi, da, ne
|
1. DA
2. NE 3. EPI |
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the affinity of ENT/OCT3
|
1. EPI
2. NE 3. DA |
|
t/f
uptake 2 also is energy, temp dependent and saturable |
f
none |
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about 70% of the the inactivation of the adrenergic neurotransmission is due to
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ezymatic: uptake recycled to vesicles
|
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which enzyme is found postganglionic
|
COMT
|
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which enzyme is found preganglionic
|
MAO
|
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what does autonomic cotransmission refer to
|
there's a transmitter and a peptide being being released
|
|
the rat vas deferens was -----
|
biphasic
this is how co transmission was discovered |
|
what else is released other than norepi?
|
ATP
|
|
what does NE work on
|
A1
|
|
receptors for ATP
|
P2X
P2Y P1 presynaptic receptors |
|
how much norepi is oxidized by MAO
|
about 20%
|
|
how do you measure sympathetic activity
|
check urine
inactive metabolite excreted in urine |
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in bl vessels what's cotransmitted w/ NE
|
NPY
|
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what are the recptors for NE in the bl vessels
|
A1
A2 |
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what are the receptors for NPY in the bl vessels
|
Y1-Y5 postsynaptic
Y2 presynaptic |
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name some peptides that ACH is cotransmitted w/ in the cholinergic system
|
VIP: brain/GI
CCK: brain/GI CGRP |
|
name some other peptides in the cholinergic system
|
somatostatin
substance P enkephalins GNRH Galanin |
|
the drive for the sympathetic system
|
CNS
|
|
what's the purpose of cotransmission
|
catecholamines have cause quick response are short
peptides prolong cuz have slower metabolism: so they last longer; maintain the contraction |
|
the localized control of release of neurotransmission
|
presynaptic receptors
|
|
prerecptor
what does A2 inhibit |
Norepi
|
|
prereceptor
B2 stimulate the release of ---- |
NE
|
|
preceptor
P1 responds to ---- what does this inhibit |
adenosine
norepi |
|
presyn.
D2 inhibit -- release |
NE
|
|
presyn
angiotensin 2 (A1) stimulate --- |
NE
|
|
presyn:
opiates (M and ENK) only inhibit release |
f
inhibit or stimulate. it depends on the type of receptor + or - |
|
presyn
prostaglandin's inhibit/stimulate release |
both
|
|
presyn
M2/M4 |
inhibit release
|
|
presyn
5HT what acts on the 5HT |
inhibit
serotonin |
|
presyn
Y2 inhibit release of what works on Y2 |
NE and NPY
NPY works on Y2 |
|
presyn
what inhibits the release of histamine |
H3
|
|
sites affecting neutrotransmission
|
sythesis
transport into the vesicle slow/rapid displacement prevent release uptake block reuptake MAO blockade COMT blockade recetpors: agonist/antagonist |
|
what will interfere w/ NE synthesis
|
a-methyl-p-tyrosine
methyldopa disulfiram |
|
what will a-methyl-p-tyrosine
inhibit |
TH
|
|
what will methyldopa inhibit
|
LAAD
|
|
what will inhibit D beta H
|
disulfram
|
|
what will block transport out of a vesicle
|
reserpine
|
|
what will slow displacement out of the vesicles
|
guanethadine
|
|
what will have rapid displacement: it will stimulate NE from nerve terminals
|
amphetamine
tyramine ephedrine |
|
what's the prob w/ rapid displacement
|
hyper then crash
|
|
what prevents release
|
bretylium
guanethadine |
|
uptake 1 blockade: prevents transport back into receptor
|
cocaine
desipramine tricyclic antidepressants |
|
enzyme blockage
|
pargyline
tropolone |
|
which med blocks mao?
comt |
mao: pargyline
comt: tropolone |
|
parkinson's is selective for
|
mao
|
|
why is cocaine addictive
|
works on DA
|