NT Systems Flashcards

1
Q

Dopamine

A
Central Location - basa ganglia and VTA
Functions - motor control, pleasure, consciousness  
Inonotropic R - none
Metabotropic R - D1, D2, D3, D4, D5
Other - tyrosine derivative
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2
Q

Norepinephrine

A

Central Location - pons/brainstem (locus cerules)
Functions - wakefulness
Iontropic R - none
Metabotropic R - alpha and beta drenergics
Other - tyrosine derivatives

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3
Q

Epinephrine

A

Central Location - brainstem (adrenal medulla)
Functions - wakefulness
Iontropic R - none
Metabotropic R - alpha and beta adrenergics
Other - tyrosine derivative

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4
Q

Serotonin

A
Central Location - brainstem (raphe nucleus)
Functions - mood, wakefulness
Iontropic R - 5HT3 (vomiting)
Metabotropic R - multiple 5HT6 - mood 
Other - tryptophan derivative
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5
Q

Histamine

A
Central Location -  hypothalamus (tuberomammillary body)
Functions - waking 
Iontropic R - none
Metabotropic R - H1 and H2 
Other - histidine derivative
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6
Q

Acetylcholine

A
Central Location - pons/midbrain
Functions - consciousness, wakefulness, voluntary motion, REM sleep  
Ionotropic R - nicotonic (sodium)
Metabotropic R - muscarinic
Other - separate from ANS
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7
Q

GABA

A

Central Location - higher CNS (cerebellum, cortex, retina)
Functions - motor control, consciousness, major inhibitory NT in CNS
Ionotropic R - GABA-A
Metabotropic R - GABA-B
Other - extrasynaptic R (anesthetics)

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8
Q

Glycine

A
Central Location - spinal cord 
Functions - almost all inhibition 
Ionotropic R - glycine (Cl) 
Metabotropic R - none
Other - none
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9
Q

Opioids

A

Central Location - hypothalamus/medulla, raphe nuclei
Functions - modulation of pain and production of pleasure
Ionotropic R - none
Metabotropic R - mu, kappa, delta
Other - endorphins, dynoprphins, enkephalins

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10
Q

Endocannibinoids

A
Central Location - multiple/Wid espread
Functions - modulation of pain/Neuroprotection
Ionotropic R - none
Metabotropic R - CB1 and CB2
Other - anandaminde and 2-AG
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11
Q

synthesis of dopamine, NE, and Epi

A

tyr to L DOPA by tyrosine hydroxylase (rate limiting)
dopamine
conversion of dopamine to NE w/in vesicles
conversion of NE to Epi w/in cytoplasm

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12
Q

substantia nigra dopaminergic pathway

A

motor control

defect leads to Parkinson’s disease

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13
Q

mesolimbic dopaminergic pathway

A

core of pleasure/reward

defect leads to addiction

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14
Q

mesocortical dopaminergic pathway

A

attention and higher levels of consciousness

defect leads to schizophrenia

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15
Q

tuberoinfundibular dopaminergic pathway

A

suppression of prolactin release from ant. pituitary

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16
Q

Reserpine

A

limits the amount of monoamines packaged into vesicles and is used in treatment of hypertension

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17
Q

D1 and D5

A

Gs

voluntary motion control

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18
Q

D2-D4

A

Gi

inhibition of voluntary motion, pleasure/reward system

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19
Q

Removal from synaptic cleft - Dopamine, NE, Epi

A

MAO - central

COMT - periphery

20
Q

Removal from synaptic cleft - Serotonin

A

MAO after uptake

21
Q

H1 and H2 R

A

mediate neuronal effects

22
Q

H3 R

A

presynaptic and decrease the release of histamine from presynaptic terminal

23
Q

Removal from synaptic cleft - Histamine

A

diamine oxidase breaks down after uptake

24
Q

Storage of ACH

A

clear vesicles

moved into vesicles by vAchT

25
Q

Removal from synaptic cleft - ACH

A

acetylocholinesterase bound to postsynaptic cell membrane

26
Q

Muscarinic R

A

blocked by atropine

smooth mm and glands

27
Q

M1

A

neuronal

increased IP3/DAG leading to increased Ca influx

28
Q

M2

A

cardiac

decreased cAMP leading to increased K efflux

29
Q

M3

A

smooth mm of bronchi, vasculature, endothelial cells of vasculature
increased IP3/DAG leading to increased Ca influx

30
Q

M4

A

glands

decreased cAMP leading to increased K efflux

31
Q

M5

A

increased IP3/DAG leading to increased Ca influx

32
Q

nicotinic R

A

located at: NMJ, autonomic ganglia

allow for Na and some Ca influx

33
Q

Stiff Person Syndrome

A

due to autoimmunity to GAD which leads to increased GABA leading to mm rigidity and mm spasms

34
Q

GABA A R

A

allow Cl into the cell causing hyperpolarization

activated by benzodiazepine

35
Q

GABA B R

A

decreased adenylyl cyclase leads to K efflux
decreased IP3/DAG leaded to decreased Ca influx
both lead to hyperpolarization

36
Q

Removal from synaptic cleft - GABA

A

Na/Cl cotransport then broken down by GAGA transaminase

37
Q

Glycine R

A

allows Cl into the cell causing hyperpolarization

blocked by strychnine

38
Q

Mu R

A

analgesia
respiratory depression
euphoria
increases K efflux leading to hyperpolarization

39
Q

Kappa R

A

analgesia

decrease Ca influx leading to hyperpolarization

40
Q

Delta R

A

analgesia

decrease Ca influx leading to hyperpolarization

41
Q

Endocannaboinoids - hippocampus

A

memory formation

42
Q

Endocannaboinoids - basal ganglia

A

affect/motor

43
Q

Endocannaboinoids - spinal cord

A

modulation of nociception (pain perception)

44
Q

Endocannaboinoids - neocortex

A

neuropcrotecive

45
Q

CB - 1 R

A

axons presynaptic terminals
Gi
reduces NT

46
Q

CB - 2 R

A

microglia
anti - inflammatory
macrophages to remove beta amyloid