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Psych 115 > Midterm 1 - Psychopharmacology > Flashcards

Midterm 1 - Psychopharmacology Flashcards

1
Q

3 Things That Can Happen to a NT When It’s Released

A
  1. Diffuse Away
  2. Broken down with enzymes
  3. Re-Uptake
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2
Q

MAOs (A&B)

(Enzyme Deactivation)

A

Enzyme that destroys excess amounts of NT by inactivating it.

Not only do MAOs break apart NTs, they re-package them so they are ready to go to the synaptic cleft and be released again.

Ex. MAOb breaks down excess dopamine. Deprenyl is a dopamine agonist because it destroys MAOb (which breaks it down in the first place).

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3
Q

SNAP-25

A

A protein that, when activated by Ca2+, drags the vesicle to the appropriate docking location on the pre-synaptic membrane.

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4
Q

Pinocytosis

A

Reuptake (the process of the membrane pinching off and becomming a re-packaged vesicle).

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5
Q

Exocytosis

A

Release

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6
Q

2 Main Drug Classifications

A
  1. Agonist
  2. Antagonist
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7
Q

Agonist

A

A drug that increases the action of the synapse/NT.

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8
Q

3 Ways A Drug Can Be An Agonist

A
  1. It can mimic the NT.
  2. It can promote release of the NT.
  3. It can block re-uptake of the NT.
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9
Q

Amphetamine

A

Dopamine agonist (mimics dopamine).

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10
Q

SSRI

A

BLOCKS RE-UPTAKE

E.g., Prozac

Developed because other antidepressants on the market would block re-uptake of serotonin AND norepinephrine. But nor-epinephrine blockers are good for lethargic depressed people, but not anxious depressed. Therefore, SSRIs do away with the norepi component.

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11
Q

Antagonist

A

A drug that decreases the function of the NT at the synapse.

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12
Q

How Does an Antagonist Work?

A

BLOCKS the post-synaptic receptors (therefore NT can’t bind to the receptor and open the ion channel).

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13
Q

Anti-Psychotics

A

Dopamine antagonists.

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14
Q

3 Classes of NTs

A
  1. Quaternary Amine
  2. Monoamines
  3. Amino acids
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15
Q

Acetylcholine (ACh)

A

Quaternary Amine

Movement workhorse.

Main NT of the muscular system. Operates at neuromuscular junction.

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16
Q

2 Categories Monoamines

A
  1. Catecholeamines
  2. Indoleamines
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17
Q

Catecholeamines

(3)

A

Dopamine

Norepinephrine

Epinephrine

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18
Q

Indoleamines

A

Serotonin

Melatonin

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19
Q

Catecholeamine Synthesis Pathway

A

Mediated by enzymes.

  1. L-Tyrosine
  2. L-Dopamine
  3. Dopamine
  4. Norepinephrine
  5. Epinephrine
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20
Q

Indoleamine Synthesis Pathway

A
  1. L-Tryptophan
  2. 5-Hydroxytryptophan
  3. 5-Hydroxytryptamine (5-HT) *Serotonin
  4. Melatonin
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21
Q

Factories in the Midbrain That Make NTs

A
  1. Substantia Nigra - dopamine (nigrostriatal pathway)
  2. Raphe Nuclei - 5-HT
  3. Ventral Tegmental Area - dopamine (median forebrain bundle)
  4. Locus Ceruleus - Norepinephrine
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22
Q

Nigrostriatal Pathway

A

Dopamine pathway that starts in the substantia nigra and ends in the striatum (starts and stops movement).

Parkinson’s

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23
Q

Median Forebrain Bundle (MFB)

A

Dopamine pathway that starts in the midbrain (VTA) and goes to the forebrain (PFC).

***Thoughts and emotions. Thought disorders.

***Schizophrenia and bipolar (mania = too much dopamine).

Without dopamine in PFC, you lose executive functioning.

24
Q

Norepinephrine

A
  • Locus Ceruleus
  • Level of game
  • Over-productivity = anxiety
  • Role in controlling brain wave functions when you sleep (wake up when norepi is released).
  • Will increase when in danger
25
Q

Raphe Nuclei

A

Makes 5-HT which goes just about everywhere.

26
Q

Tectum

A

Roof of midbrain.

27
Q

Tegmentum

A

Floor of midbrain.

28
Q

Amino Acid NTs

(3)

A

Most prevalent NTs in the brain! A majority of brain function is conducted from the release of glutamate and GABA.

  1. Glutamate
  2. GABA
  3. Glycine
29
Q

Glutamate

A

AA NT

  • Always excitatory
  • Primary NT in the brain!
30
Q

GABA

A

AA NT

  • Always inhibitory
31
Q

Glycine

A

AA NT

  • Inhibitory
32
Q

Dopamine Agonist

A

Stimulant

  • Meth = Mimics dopamine
  • Cocaine = Selective Dopamine Re-Uptake Inhibitor
33
Q

Dopamine Antagonist

A

Opposite of a stimulant

  • Anti-psychotic (Thorazine, Haldol, Chlorpromazine)
  • Interrupts transmission to median forebrain bundle
  • Problem = Movement disorders (dopamine initiates movement). Parkinsonian like symptoms.
34
Q

5-HT Agonist

A
  • Increases serotonin
  • Increases mood, decreases appetite, makes sleepy, gives hallucinations
  • Hallucinogens
35
Q

5-HT Antagonist

A

Depressant.

Experimental only (may block hallucinations)

36
Q

GABA Agonist

A

Increases inhibition.

  • Barbituates
  • Benzos - works on GABAa and will compete with alcohol (mimic GABA and let Cl- in) (creates IPSP)
  • Alcohol - works on GABAa and will compete with benzos

Inhibitory NTs let in negatively charged ions.

37
Q

GABA Antagonist

A

Excitatory

No known GABA antagonists.

38
Q

Glutamate Agonist

A

Stimulant

  • No known drugs that act as GA.
39
Q

Glutamate Antagonist

A
  • Anesthetics (put to sleep but doesn’t paralyze)
  • E.g., propophol
40
Q

ACh Agonist

A
  • Increased motor function and firing at neuromuscular junction.
  • Overexcites heart muscles.
  • Spider and snake venom
  • POISON
41
Q

ACh Antagonist

A
  • Paralyzes
  • Muscles get too relaxed and stop working
  • Botulism
42
Q

L-DOPA

A

Parkinson’s drug that increases synthesis of dopamine in the nigrostriatal pathway.

43
Q

Dopamine Receptors

A
  • Branch 1 = D1, D2, D3
  • Branch 2 = D4-D5
44
Q

Dopamine D2 Receptor

A
  • Key movement receptor in striatum
  • D2 Antagonist blocks motor function
45
Q

D4 Dopamine Receptor

A
  • Found in forebrain
  • D4 Antagonist blocks hallucinations without blocking movement.
46
Q

5-HT Receptors

A

1-17

47
Q

5-HT 3,4 Receptors

A

Satiety

48
Q

5-HT 2a

A

Responsible for hallucinations. Active site for hallucinogens.

LSD, MDMA act on these receptors

49
Q

MDMA

A

Promotes release of dopamine and can mimic dopamine.

Can also increase the release of 5-HT.

Therefore, it’s a combination dopamine and 5-HT agonist.

*Breaks down to meth in brain.

50
Q

Most Common Receptors in the Brain

A

G-Protein coupled receptors

51
Q

G-Protein Coupled Receptor

A
  • Transmembrane
  • NT will bind and activate G-Protein on bottom, inside cell receptor.
  • This part that’s inside can send signals to other channels to open.
  • Amplifies signal.
52
Q

Hormones vs. NTs

A

Hormones

  • Large
  • Can go a long distance

NTs

  • Small
  • Only travel across synapses

***Both can alter behavior!

53
Q

Endogenous Opioids

A

Endorphins, Enkaphalines

54
Q

How do synapses maintain homeostasis?

A

Up-regulating and down-regulating post-synaptic receptor sites.

55
Q

Down-Regulation vs. Up-Regulation

A

Down-Regulation

  • Tolerance b/c receptors go down beneath surface so NTs/Drugs can’t find receptors (therefore have to take more and more = tolerance)

Up-Regulation

  • Response to withdrawal
56
Q

Tolerance

A

Neuron will get over-excited and compensate by down-regulating

(e.g., In meth, there’s way more release of dopamine)

57
Q

Withdrawal

A

When stop taking drug, receptors will up-regulate (peak head back out to look for NT in synaptic cleft).

Withdrawal lessens with up-regulation

Psych 115 (12 decks)

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