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Neuroscience I > Karius- Neurotransmitter Systems > Flashcards

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?

A

GABA-b

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
Q

where is glycine found?

A

spinal cord*, brainstem, forebrain (SC most important)

25
Q

what is the fxn of glycine?

A

mediates spinal inhibitions

26
Q

what kind of receptor is glycine receptor?

A

ionotropic

27
Q

what kind of channel is Glycine receptor?

A

Cl- channel

28
Q

what blocks glycine receptor?

A

strychnine

29
Q

what are the peptide NTs?

A

opoids and endocannabinoids

30
Q

what are opoids responsible for?

A

emotion and pleasure

31
Q

where are opoids located?

A

basal ganglia, hypothalamus, parabrachial & raphe nuclei

32
Q

what is the fxn of opoids?

A

modify nociceptive inputs and mood/affect

33
Q

what are the 4 precursors for opoids?

A

proenkephalin, POMC (ACTH precursor), Prodynorphin, & Orphanin FQ (aka nociceptin)

34
Q

how are opoids limited?

A

enzymatic, possibly after reuptake with Enkephalinase A&B and aminopeptidases

35
Q

opoid receptors are what kind? lead to?

A

GPCR, Gi, decrease AC

36
Q

what are the functions of mu opoid receptors?

A

analgesia, respiratory depression, euphoria, (also: sedation & constipation*)

37
Q

what is mu used for in medicine besides pain control?

A

respiratory depression- end of life care

38
Q

activation of kappa receptors lead to?

A

analgesia and dysphoria (also, diuresis & miosis)

39
Q

activation of delta receptors causes?

A

analgesia

41
Q

endocannabinoids have which 2 NTs? structure of each?

A 
anandamide= AA+ ethanolamine
2-Arachidonylglycerol= AA esterified in middle of glycerol
42
Q

where are endocannabinoids found?

A

hippocampus, basal ganglia, and spinal cord

43
Q

what kind of receptor is CB1?

A

Gi

44
Q

where is CB1 found? do?

A

presynaptic term of EAA and GABA synapses; decrease NT release

45
Q

where is CB2 found?

A

in brain microglia

46
Q

what has CB2 been implemented in?

A

immune system, gut, anti-inflammatory effects

AD: Macrophages remove B-amyloid protein

Neuroscience I (20 decks)

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