Karius- Neurotransmitter Systems Flashcards

0
Q

where is Ach made?

A

midbrain, pons, striatum

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1
Q

What is Ach responsible for?

A

consciousness, REM, voluntary movement

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2
Q

who’s gonna kick neuro’s ass?

A

WE ARE

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3
Q

what limits Ach? where is it?

A

AchE (true); bound to post-synaptic membrane

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4
Q

what are the metabotropic receptors for Ach?

A

muscarinic M1-4

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5
Q

which muscarinic receptor is Gi? where is it located?

A

M2; heart

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6
Q

what is the neuronal mAchR?

A

M1

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7
Q

where is M3 found?

A

smooth m.

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8
Q

where is M4 found?

A

glands

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9
Q

which mAchRs are Gq? causes?

A

M1, 3, 4; increase IP3/Dag and increase Ca2+

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10
Q

which AchRs are ionotropic?

A

nicotinic receptors

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11
Q

iontropic receptors always have what structure? what happens if you change it?

A

5 subunits; change subtype, change behavior

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12
Q

where are nAchRs located?

A

NMJ, autonomic ganglia, CNS

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13
Q

what are the excitatory amino acids?

A

glutamate, aspartate, (and taurine)

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14
Q

what are the inhibitory amino acids?

A

GABA and glycine

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15
Q

what is GABA responsible for?

A

conciousness/awarenessd, voluntary motion (major inhibitory amino acid)

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16
Q

where is GABA located?

A

cortex, cerebellum, retina

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17
Q

how is GABA synthesized?

A

GAD (from glutamate)

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18
Q

what limits action of GABA?

A

reuptake and GABA transaminase

19
Q

what is the metabotropic GABA receptor?

20
Q

what is the ionotropic GABA receptor? what does it conduct? what does this lead to?

A

GABA-a, Cl- conductance, hyperpolarization

21
Q

what is unique about GABAaR?

A

benzodiazepine site; extrasynaptically thought to involved in anesthetics

22
Q

what is the structure of GABAbR?

A

heterodimer of Gq and Gi

23
Q

what does activation of GABAbR lead to?

A

decrease AC, increase K efflux, decrease IP3/DAG, decrease Ca influx—-> hyperpolarization

24
where is glycine found?
spinal cord*, brainstem, forebrain (SC most important)
25
what is the fxn of glycine?
mediates spinal inhibitions
26
what kind of receptor is glycine receptor?
ionotropic
27
what kind of channel is Glycine receptor?
Cl- channel
28
what blocks glycine receptor?
strychnine
29
what are the peptide NTs?
opoids and endocannabinoids
30
what are opoids responsible for?
emotion and pleasure
31
where are opoids located?
basal ganglia, hypothalamus, parabrachial & raphe nuclei
32
what is the fxn of opoids?
modify nociceptive inputs and mood/affect
33
what are the 4 precursors for opoids?
proenkephalin, POMC (ACTH precursor), Prodynorphin, & Orphanin FQ (aka nociceptin)
34
how are opoids limited?
enzymatic, possibly after reuptake with Enkephalinase A&B and aminopeptidases
35
opoid receptors are what kind? lead to?
GPCR, Gi, decrease AC
36
what are the functions of mu opoid receptors?
analgesia, respiratory depression, euphoria, (also: sedation & constipation*)
37
what is mu used for in medicine besides pain control?
respiratory depression- end of life care
38
activation of kappa receptors lead to?
analgesia and dysphoria (also, diuresis & miosis)
39
activation of delta receptors causes?
analgesia
41
endocannabinoids have which 2 NTs? structure of each?
``` anandamide= AA+ ethanolamine 2-Arachidonylglycerol= AA esterified in middle of glycerol ```
42
where are endocannabinoids found?
hippocampus, basal ganglia, and spinal cord
43
what kind of receptor is CB1?
Gi
44
where is CB1 found? do?
presynaptic term of EAA and GABA synapses; decrease NT release
45
where is CB2 found?
in brain microglia
46
what has CB2 been implemented in?
immune system, gut, anti-inflammatory effects | AD: Macrophages remove B-amyloid protein