Neurotransmitter Review Flashcards

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1
Q

Molecular structure of Ligand-gated ion channels

A

4 transmembrane regions of a subunit, 4-5 subunits combine to form a channel.

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2
Q

GPCR Structure

A

Single polypeptide with 7 TM domains

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3
Q

Neurotrophic factor reception

A

Usually dimerized receptors that are TKs.

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4
Q

Major excitatory NT

A

Glu, very ubiquitous and only a minute fraction is packaged into vesicles.

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5
Q

Two types of Glu receptors

A

Ligand Gated Na/Ca channels = AMPA, NMDA, Kainate

GPCR = mGluR 1-8 (Modulatory effects and autoreceptors)

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6
Q

How to astrocytes regulate glutamatergic transmission?

A

They buffer synaptic glutamate levels and protect nearby neurons from excitotoxicity. Astrocytes take up glutamate using GLT-1 (also transport K and Na).

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7
Q

Major inhibitory NT

A

GABA, 40-50% of neurons use.

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8
Q

Two major classes of GABA receptors

A

Ligand gated Cl channels = GABAa

GPCR= GABAb (modulatory effects and autoreceptors).

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9
Q

How is GABA synthesized?

A

It is made from glutamate via glutamic acid decarboxylase, and degraded by GABA transaminase.

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10
Q

How do sedative hypnotics (Benzos, barbiturates, alcohol) work?

A

By promoting the activity of GABAa receptors.

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11
Q

How do anticonvulsant drugs (like vigabatrin) work?

A

By promoting GABA synthesis or preventing its degradation/reuptake.

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12
Q

Major inhibitory NT in spinal cord?

A

Glycine

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13
Q

How to induce seizures?

A

Glycine receptor antagonists, like strychnine.

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14
Q

Class of glycine receptors

A

Strychnine-sensitive glycine receptor (ligand gated Cl- channel)

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15
Q

What else is glycine good for?

A

Co-agonist for NMDA receptor (not responsive to strychnine)

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16
Q

Catecholamine degradative enzymes

A

MAO and COMT

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17
Q

Catecholamine synthesis pathway

A

Tyrosine (TH) L-DOPA (AADC) Dopemine (DBH) NE (PNMT) E

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18
Q

Three major dopaminergic pathways in brain

A

1) Nigrostriatal (movement)
2) Mesocorticolimbic (VTA to NAcc) – motivation/addiction/emotion
3) Tuberoinfundibular (Arcuate nucleus to anterior pituitary) – prevents release of prolactin

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19
Q

Dopamine Receptors

A

All GPCR

D1, D5 – Gs

D2, D3, D4 –Gi, autoreceptors

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20
Q

Antipsychotic drug action

A

D2 antagonists.

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21
Q

Psychostimulant (meth, cocaine, ritalin)

A

Inhibit reuptake or stimulate release of DA.

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22
Q

Treatment of PD

A

L-DOPA or D2 agonists.

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23
Q

Noradrenergic projections

A

Locus ceruleus and other brainstem nuclei to cortex, cerebellum, and tectum.

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24
Q

Noradrenergic receptors

A

All are GPCR

B – GS
a1 – gq
a2– gi (autoreceptor)

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25
Q

Antidepressant drug effect on NE

A

Suppress reuptake

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26
Q

Synthesis of serotonin/melatonin

A

Tryptophan (tryptophan hydroxylase) 5HTP (AADC) 5HT (5HT N-acetylase) 5HT N-acetylase (5hydroxyindole o methyltransferase) melatonin

27
Q

Where is melatonin utilized?

A

Pineal gland. Function unknown.

28
Q

Serotonergic Projections start from…

A

Dorsal raphe nucleus (midbrain)

29
Q

5HT receptors

A

5HT1 – Gi, autoreceptor
5HT2 – Gq
5HT3 – ligand gated
5HT4-7 – Gs

30
Q

Functions of serotonin

A

Regulating stress responses and emotional behavior, regulating eating/weight control

31
Q

How do antidepressants affect 5HT

A

Prevent reuptake

32
Q

New antipsychotic drugs

A

D2 antagonists, but also block 5HT2a receptors.

33
Q

Hallucinogens

A

5HT2a partial agonists

34
Q

Antimigrane Drugs (triptans)

A

5HT1d agonists.

35
Q

Acetylcholine synthesis

A

Choline + Acetyl CoA (Choline acetyltransferase) Acetylcholine (AChE) Choline + Acetate

36
Q

Most important ACh Projection in brain

A

Hippocampus

37
Q

Acetylcholine in striatum?

A

yes in interneurons

38
Q

Acetylcholinergic projections

A

1) Basal forebrain nuclei (medial septal nucleus, diagonal band, nucleus basalis) project to hippocampus and are important for cognition.
2) Brainstem nuclei (dorsolateral tegmentum in pons) project widely and are important for sleep.

39
Q

Why is smoking addictive?

A

Nicotine is a strong partial agonist at central nicotinic cholinergic receptors, which activate dopaminergic neurons in the VTA

40
Q

Acetylcholine and PD

A

mAChR antagonists used to treat PD (work via striatal circuits), also D2 agonists.

41
Q

AChE inhibitors treat?

A

Treat dementia (via hippocampal circuits)

42
Q

Side effects of ACh antagonists

A

tachycardia, dry mouth, blurred vision

43
Q

Botox

A

Blocks ACh release

44
Q

Curare

A

Blocks NMJs.

45
Q

Histamine Synthesis

A

From histidine (histidine decarboxylase) histamine

46
Q

Where is histamine used?

A

Used solely by the tuberomammilary nucleus in hypothalamus.

47
Q

Histamine receptors

A

All GPCR

H1 – most important in brain
H2 – inhibits stomach acid
H3 – autoreceptor

48
Q

Function of histamine in CNS

A

Promotes sedation

49
Q

Where does peptide synthesis occur?

A

Cell body, must be transported. Also enzymatically degraded (irreversible)

50
Q

What type of receptors do peptide NTs use?

A

GPCRs only

51
Q

Types of peptide NTs

A

Hypothalamic factors (CRF, TRF, GnRF)
Feeding and Gut peptides (NPY, cholesystokinin, VIP)
Tachykinins (substance p–nociception)

52
Q

Orexin used where?

A

Lateral hypothalamus, but widespread projections

53
Q

Orexin receptors

A

OX1, OX2 (GPCR)

54
Q

Function of Orexin

A

Wakefulness

55
Q

Narcolepsy

A

caused by death of orexigenic neurons

56
Q

Three opioid peptides

A

Enkephalins (preproenkephalin)
Endorphins (POMC)
Dynorphin (preprodynorphin derived)
Mu delta kappa

57
Q

Nucleoside NTs

A

ATP released with most NTs, converted to adenosine in synaptic space, many different receptors.

58
Q

Adenosine function

A

Accumulates during wakefulness to promote sleep, sleep reduces adenosine levels

59
Q

Caffeine

A

Adenosine receptor antagonist.

60
Q

Endocannabinoids

A

Anandamide and 2-AG

61
Q

Synthesis of endocannabinoids

A

Synthesized postsynaptically in response to Ca influx, then released into synapse to act on CB1 and CB2 receptors on presynapse.

62
Q

NO as a NT

A

Synthesized postsynaptically by NO synthase which is activated by Ca, diffuses to presynapse where it activates cyclic GMP to modulate NT release

63
Q

Main function of retrograde messengers

A

Modulate NT release.