NTM DSA Flashcards by Liz Pennington

What are the monoamines?

epinephrine

norepinephrine

dopamine

serotonin

histamine

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Where do you find norepinephrine

locus ceruleus

pontine/medullary areas

does wake/alert stuff

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Where do you find epinephrine?

medulla

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How is epinephrine/norepinephrine made?

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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Where do you find dopamine?

basal ganglia (motor control)

hypothalamus/limbic (endrocine/emotional control)

cortex

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Dopamine reuptake?

binds to?

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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Where do you find serotonin?

hypothalamnus and limbic system (mood)

brainstem raphe nuclei (motor)

cerebellum (motor)

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How do you make serotonin?

reuptake?

from tryptophan via tryptophan hydroxylase

catabolism by MAO and COMT

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serotonin receptors

several, one ionotropic receptor that increases Na

5HT3-area postrema

5HT6-antidepressant

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Where do you find histamine?

tuberomamillary nucleus of hypothalamus (keeps you awake)

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How do you make histamine?

how to you uptake histamine?

from histidine via histidine decarboxylase

catabolism by diamine oxidase and COMT

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Histamine receptors

H1-PLc activcation, wakefulness

h2: increase cAMP

h3-decreases histamine release

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Where is Ach made?

the striatum of the basal ganglia (caudate and putamen)

midbrain and pons

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functions of Ach

basal ganglia: control voluntary movement

MB/pons: excite cortex, REM sleep

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Ach synthesis

choline and acetate

moved into vesciles via VAchT

removed from synapse via Achesterase

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Ach muscarinic receptors

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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Ach nicotinic receptors

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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What is the major inhibitory amino acid NTM

GABA

wildly distributed in cortex, cerebellum, BG

critical for cinsciouness, motor control and vision

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GABA synthesis

made from glutamate via GAD

transported to vescile via VGAT and removed from synapse via GAT

GAT1-presynaptic

GAT2-glial cells

What does GAT 2 do?

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

GABAa receptors

ionotropic

produces IPSP

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

many extrasunaptic GABA receptors, used for anasthetics

GABAb receptors

metabotropic

increases K+, shuts down Ca+

presynaptic-regulates NTM release

postsynaptic-inhibits postsynaptic cell

glycine found in

functions

made from

uptake

spinal cord

brainstem/medulla

mediates spinal inhibitions

AA (it is one)

GAT/recycling

glycine receptor

ionotropic

Cl- causes IPSP

modified by ETOH and general anesthetics and potentiates

stychnine binds and blocks

Where are the purines found and what are they?

ATP, ADP, adenosine cortex cerebellum hippocampus BG

P1: adenosine pre-synaptic for inhibiton of NTM release post-synaptic for sleep and neuronal function inhibition

P2X-ionotropic, ATP P2Y-metabortropic, Gi/Gq, ATP, ADP, UTP, UDP functions in learning, memory, modification of locomotion

What are the types of opioids?

endorphins (endogenous morphine) enkephalins dynorphins nociceptin

Where do we find opioids?

THE ER! (just kidding) basal ganglia hypothalamus pontine/medulla

functions of the opioids

modify nociceptive input (analgesia) mood/affect

removal of opioids

reuptake enzymatic destruction by enkephalinase and aminopeptidase

opioid receptor: Mu receptor

metabotropic analgesia resp. depression euphoria constipation sedation

opioid receptors: Kappa receptors

serpentine analagesia dysphoria diuresis miosis

Opioid receptors: delta receptors

serpentine analgesia ONLY

How do the opioid receptors work?

all connect to Gi/Go Mu: increase K efflux and cause hyperpolarization delta/kapp: decrease Ca influx

What are the endogenous cannabinoids found where?

anadamide 2-arachiondylaglycerol basal ganglia (mood/motor) spinal cord (nociception) cortex (neuroprotection) hippocampus and hypothalamnus

where do the endocannabinoids come from?

derived from arachinodinc acid occurs in presynaptic terminal anadamide comes from NAPE 2-AG from PIP2

CB1 importance

associated with psychoactive repsonses to cannabinoids polymorphisms linked to obesity, ADHD, schizo., Parkinson's

CB1 found uniformly here CB1 found non-uniformly here

striatum thalamus hypothalamus cerebellum lower brain stem cortex, amygdala, hippocampus

where are the cannabinoid receptors located?

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

CB2

found on microglia highly inducible in response to injury or inflammation

degradation of the endocannabinoids

hydrolysis or oxidation AEA can undergo fatty acid hydrolase or oxidation 2AG can undergo MAGL or oxidation

excitatory amino acids glutamate aspartate

from a-kg localized with glitamate, in visual cortex and pyramidal cells

NMDA and Non NMDA

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

overview functions of NMDA and non NMDA

NMDA used in short and long term memory and synaptic plasticity nonNMDA used in sensory afferents, upper motor neurons, etc.

NMDA and NO synthesis

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

neural functions of NO

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)