Phys - Neurotransmitters Flashcards

1
Q

location of cell bodies in the CNS that release NE

A

locus ceruleus

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2
Q

location of cell bodies in the CNS that release epinephrine

A

brainstem

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3
Q

location of cell bodies in the CNS that release serotonin

A

raphe nuclei

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4
Q

location of cell bodies in the CNS that release histamine

A

tuberomammillary nucleus

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5
Q

location of cell bodies in the CNS that release dopamine

A

VTA (ventral tegmental area)

SNPC (substantia nigra pars compacta)

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6
Q

function of NE

A

movement from awake –> awareness

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7
Q

what are the receptors for NE and what G protein pathway do they use

A

alpha 1: Gq

alpha 2: Gi

beta: Gs

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8
Q

function of dopamine

A

crucial in creating alertness

voluntary motion

pleasure

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9
Q

receptors for dopamine and the G protein pathways they use

A

D1: Gs

D2 and D3: Gi

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10
Q

functions of serotonin

A

“quiet awareness”

modulation of pain

mood and affect

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11
Q

what is the ionotropic receptor for serotonin and what does its activation do

A

5HT3

–> allows influx of Na+

–> vomiting reflex

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12
Q

what are the metabotropic receptors for serotonin

A

5HT1, 2, 4, 5, 6, 7

(5HT3 is ionotropic)

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13
Q

location of cell bodies in the CNS that produce ACh

A

pons and midbrain

striatum of basal ganglia

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14
Q

compare ACh functions when it originates in the brainstem (midbrain and pons) and in the striatum of basal ganglia

A

midbrain and pons: arousal and REM sleep

basal ganglia: motor control (voluntary motion)

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15
Q

describe what occurs when the ionotropic (nicotinic) receptors of ACh are activated

A

mostly Na+ transport with a small amount of Ca2+, but still more Ca2+ than in the periphery

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16
Q

what is the major metabotropic receptor for ACh

A

M1

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17
Q

what G protein pathway does M1 receptor for ACh stimulate

A

Gq

–> increased IP3/DAG –> increased Ca2+

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18
Q

what G protein pathway does M4 receptor for ACh stimulate

A

Gi

–> decreased cAMP

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19
Q

what G protein pathway does M5 receptor for ACh stimulate

A

Gq

–> increased IP3/DAG –> increased Ca2+

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20
Q

serotonin is a derivative of what amino acid

A

tryptophan

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21
Q

what are the *critical* roles of GABA

A

consciousness

motor control

vision (retina)

22
Q

what is GABA made from and what is the rate limiting enzyme in its synthesis

  • how is GABA transported into vesicles
  • how is GABA removed from synapse
A

from glutamate

glutamate decarboxylase (GAD)

tranported: vesicular GABA transporter protein (VGAT)
removed: GABA transporter (GAT)

23
Q

where are GAT1 and GAT2 located and what do they do

A

GAT1: on presynaptic terminal

GAT2: on glial cells surrounding synapse

  • both remove GABA from the synapse
24
Q

what happens to GABA if it is taken up by GAT1

A

it is repackaged into vesicles as is

25
what happens to GABA if it is taken up by GAT2
GABA is converted to glutamine and released to the ECF --\> will then be taken up by presynaptic terminal and recycled into GABA
26
activation of GABA-A receptors causes what
Cl- conductance --\> IPSP (in adult neurons) ## Footnote **(ionotropic receptor)**
27
activation of GABA-B receptors causes what
activation of K+ (GIRK) channel and inhibition of Ca2+ channel
28
compare function of GABA-B receptors when presynaptic and when postsynaptic
presynaptic: regulates NT release postsynaptic: inhibition of post-synaptic cell **(metabotropic receptor)**
29
location of cell bodies in CNS that release GABA
higher CNS
30
location of cell bodies in CNS that release glycine
major: spinal cord brainstem (medulla)
31
function of glycine
mediates many spinal inhibitions
32
how is glycine removed from the synapse
by either GAT proteins or recycling
33
what is the only receptor for glycine and what does it do
GlyR - ionotropic - allows chloride to influx leading to IPSP
34
compare what happens when ethanol and anesthetics bind to GlyR and when stychnine binds to GlyR
ethanol and anesthetics: potentiate its effects stychnine: blocks it
35
what protein stores purines (ATP, ADP, adenosine) in vesicles
VNUT protein
36
where are purines found in the CNS
virtually everywhere, especially: - cortex - cerebellum - hippocampus - basal ganglia
37
P1 receptor for purines - what is its ligand - what does it do when located presynaptically - what does it do when located postsynaptically
adenosine presynaptic: inhibition of neurotransmitter release postsynaptic: sleep induction, inhibition of neural function
38
what occurs when P2 receptors are activated for purines
learning and memory modiciation of locomotor pathways
39
what are the ligands for: the P2X receptor for purines the P2Y receptor for purines
P2X: ATP P2Y: ATP, ADP, UTP, UDP
40
location of cell bodies in CNS that produce opioids
basal ganglia hypothalamus pons/medulla
41
The two endogenous cannabinoids anandamide and 2-arachidonylglycerol (2AG) are derivatives of what
arachidonic acid
42
endocannabinoids in the basal ganglia control what
mood motor control
43
endocannabinoids in the spinal cord control what
modulation of nociception (pain)
44
endocannabinoids in the cortex control what
neuroprotection
45
endocannabinoids in the hippocampus control what
memory formation (disruption of)
46
endocannabinoids in the hypothalamus control what
control of body energy/hunger
47
location and function of CB1 receptors
location: pre-synaptic terminals of EAA and GABA releasing synapses function: reduces EAA and GABA release via Gi coupled protein (also binds endogenous cannabinoids)
48
what receptor do the endogenous cannabinoids bind to to cause their effects (mood, motor performance, hunger, etc.)
CB1
49
location and function of CB2 receptor
location: microglia in brain, gut, immune system function: anti-inflammatory
50
activation of the CB2 receptor by cannabinoids causes what
increased B-amyloid removal (helping Alzheimer's)
51
location of cell bodies in CNS that produce endocannabinoids
basal ganglia cortex spinal cord
52
what kind of receptor is CB1
metabotropic