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Neuroendocrine Exam 2 > NTM DSA > Flashcards

NTM DSA Flashcards

1
Q

What are the monoamines?

A

epinephrine

norepinephrine

dopamine

serotonin

histamine

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2
Q

Where do you find norepinephrine

A

locus ceruleus

pontine/medullary areas

does wake/alert stuff

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3
Q

Where do you find epinephrine?

A

medulla

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4
Q

How is epinephrine/norepinephrine made?

A

tyrosine–>dopamine–>norepi–>epi

via tyrosine hydroxylase

NE is converted to epi by PNMT

reuptake or ezymatic degradation by monoamine oxidase or catecholomethyl transferase

bind to a- or b-adrenergics

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5
Q

Where do you find dopamine?

A

basal ganglia (motor control)

hypothalamus/limbic (endrocine/emotional control)

cortex

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6
Q

Dopamine reuptake?

binds to?

A

catabolism by MAO and COMT

metabotropic receptors, increases cAMP in D1 &D5

D2: decreases cAMP, K+ increases

D3 &4: decreases cAMP

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7
Q

Where do you find serotonin?

A

hypothalamnus and limbic system (mood)

brainstem raphe nuclei (motor)

cerebellum (motor)

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8
Q

How do you make serotonin?

reuptake?

A

from tryptophan via tryptophan hydroxylase

catabolism by MAO and COMT

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9
Q

serotonin receptors

A

several, one ionotropic receptor that increases Na

5HT3-area postrema

5HT6-antidepressant

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10
Q

Where do you find histamine?

A

tuberomamillary nucleus of hypothalamus (keeps you awake)

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11
Q

How do you make histamine?

how to you uptake histamine?

A

from histidine via histidine decarboxylase

catabolism by diamine oxidase and COMT

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12
Q

Histamine receptors

A

H1-PLc activcation, wakefulness

h2: increase cAMP

h3-decreases histamine release

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13
Q

Where is Ach made?

A

the striatum of the basal ganglia (caudate and putamen)

midbrain and pons

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14
Q

functions of Ach

A

basal ganglia: control voluntary movement

MB/pons: excite cortex, REM sleep

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15
Q

Ach synthesis

A

choline and acetate

moved into vesciles via VAchT

removed from synapse via Achesterase

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16
Q

Ach muscarinic receptors

A

M1-increases Ca

M2-increases K (slows HR)

M3-increases Ca (constricts SM)

M4-decreases cAMP in striatium

M5-increases Ca in dopaminergic neurons in BG

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17
Q

Ach nicotinic receptors

A

NMJ

autonomic ganglia and other central synapses

changing subunits changes the properties of the channel, some will allow more Ca in

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18
Q

What is the major inhibitory amino acid NTM

A

GABA

wildly distributed in cortex, cerebellum, BG

critical for cinsciouness, motor control and vision

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19
Q

GABA synthesis

A

made from glutamate via GAD

transported to vescile via VGAT and removed from synapse via GAT

GAT1-presynaptic

GAT2-glial cells

20
Q

What does GAT 2 do?

A

takes up GABA and converts it to glutamine and then releases it to the ECF where it is recycled back into GABA

21
Q

GABAa receptors

A

ionotropic

produces IPSP

binding sites modualted by benzos, ETOH, steroids, all causing potentiation

many extrasunaptic GABA receptors, used for anasthetics

22
Q

GABAb receptors

A

metabotropic

increases K+, shuts down Ca+

presynaptic-regulates NTM release

postsynaptic-inhibits postsynaptic cell

23
Q

glycine found in

functions

made from

uptake

A

spinal cord

brainstem/medulla

mediates spinal inhibitions

AA (it is one)

GAT/recycling

24
Q

glycine receptor

A

ionotropic

Cl- causes IPSP

modified by ETOH and general anesthetics and potentiates

stychnine binds and blocks

25
Q

Where are the purines found and what are they?

A

ATP, ADP, adenosine

cortex

cerebellum

hippocampus

BG

26
Q

P1

A

P1: adenosine

pre-synaptic for inhibiton of NTM release

post-synaptic for sleep and neuronal function inhibition

27
Q

P2

A

P2X-ionotropic, ATP

P2Y-metabortropic, Gi/Gq, ATP, ADP, UTP, UDP

functions in learning, memory, modification of locomotion

28
Q

What are the types of opioids?

A

endorphins (endogenous morphine)

enkephalins

dynorphins

nociceptin

29
Q

Where do we find opioids?

A

THE ER! (just kidding)

basal ganglia

hypothalamus

pontine/medulla

30
Q

functions of the opioids

A

modify nociceptive input (analgesia)

mood/affect

31
Q

removal of opioids

A

reuptake

enzymatic destruction by enkephalinase and aminopeptidase

32
Q

opioid receptor: Mu receptor

A

metabotropic

analgesia

resp. depression

euphoria

constipation

sedation

33
Q

opioid receptors: Kappa receptors

A

serpentine

analagesia

dysphoria

diuresis

miosis

34
Q

Opioid receptors: delta receptors

A

serpentine

analgesia ONLY

35
Q

How do the opioid receptors work?

A

all connect to Gi/Go

Mu: increase K efflux and cause hyperpolarization

delta/kapp: decrease Ca influx

36
Q

What are the endogenous cannabinoids

found where?

A

anadamide

2-arachiondylaglycerol

basal ganglia (mood/motor)

spinal cord (nociception)

cortex (neuroprotection)

hippocampus and hypothalamnus

37
Q

where do the endocannabinoids come from?

A

derived from arachinodinc acid

occurs in presynaptic terminal

anadamide comes from NAPE

2-AG from PIP2

38
Q

CB1 importance

A

associated with psychoactive repsonses to cannabinoids

polymorphisms linked to obesity, ADHD, schizo., Parkinson’s

39
Q

CB1 found uniformly here

CB1 found non-uniformly here

A

striatum

thalamus

hypothalamus

cerebellum

lower brain stem

cortex, amygdala, hippocampus

40
Q

where are the cannabinoid receptors located?

A

pre-synaptoic

binds AEA and 2AG and reduce NTM release of GABA and excitatory NTMs

41
Q

CB2

A

found on microglia

highly inducible in response to injury or inflammation

42
Q

degradation of the endocannabinoids

A

hydrolysis or oxidation

AEA can undergo fatty acid hydrolase or oxidation

2AG can undergo MAGL or oxidation

43
Q

excitatory amino acids

glutamate

aspartate

A

from a-kg

localized with glitamate, in visual cortex and pyramidal cells

44
Q

NMDA and Non NMDA

A

ionotropic receptors

allows Ca influx

glycine is a required co-agonist

Mg can bind and block at RMP and prevent Ca influx

PCP drug can bind and block

non NMDA uses AMPA and can bind and depolarize cell and kick Mg out of binding site so that Ca can enter via NMDA, long lasting ESPS

benzos can bind to non NMDA and reduce Na entering

Kainate does the same thing

45
Q

overview functions of NMDA and non NMDA

A

NMDA used in short and long term memory and synaptic plasticity

nonNMDA used in sensory afferents, upper motor neurons, etc.

46
Q

NMDA and NO synthesis

A

NMDA allows Ca to go into cell and bind to calcineurin which activates NOS

47
Q

neural functions of NO

A

long term potentiation in hippocampus and cerebellum

CV and resp. control in pons/medulla

cytotoxic in macrophages, vasodilation

very unstable, leads to free radicals, toxic to neurons (not the ones that make it)

Neuroendocrine Exam 2 (25 decks)

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