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Neuropsychopharmacology > Week 3 - Depression > Flashcards

Week 3 - Depression Flashcards

1
Q

Brain regions involved in depression?

A

Prefrontal Cortex
Hippocampus
Amygdala

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2
Q

What happens to the affected brain regions in depression?

A

Prefrontal Cortex - reduced

Hippocampus - reduced

Amygdala - overactive

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3
Q

How did they find out about depression?

A

Iproniazid (1950’s) elevated mood in tuberculosis patients

  • Increases monoamines in synaptic cleft
  • Monoamine Oxidase Inhibitor
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4
Q

Monoamine =

A

Serotonin
Dopamine
Noradrenaline

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5
Q

What does a monoamine oxidase do?

A

Breaks down monoamines (Serotonin, Dopamine, Noradrenaline)

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6
Q

What did they find in the brain of depressed patients?

A

There are changes in monamines in the brain and that they are really important for depression

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7
Q

What is the Monoamine Hypothesis?

A

The effectiveness of a monoamine oxidase inhibitor to elevate mood in depressed patients indicated that the depletion of monoamines contributed to the
pathology of depression.

Put simply, when you inhibit the break down of serotonin etc. depressed patients feel better which suggests that they have a depletion of these things in the first place.

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8
Q

What are the Catecholamines?

A

Dopamine (DA) and noradrenaline (NA)

(they are very highly related)

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9
Q

What is the Indolamine?

A

Serotonin (5-HT)

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10
Q

What happens when you don’t eat tryptophan?

A

You won’t have enough serotonin because tryptophan makes it.

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11
Q

What is Tryptophan in?

A

is in meats, dairy and grains

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12
Q

Neurotransmitters in Mania?

A
  • > serotonin
  • > dopamine
  • > noradrenaline
  • < GABA!
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13
Q

What do Tricyclic antidepressent do?

A

block the re-uptake
of ALL monoamines

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14
Q

What does Monoamine Oxidase Inhibitors?

A

block the metabolism of ALL monoamines

  • Depressed people have reduced monoamine levels
  • MAOI’s restore the monoamine levels to ‘normal’
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15
Q

What is an MAOI

A

Monoamine Oxidase Inhibitors

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16
Q

What are the treatments for depression?

A
  • Tricyclic
  • Monoamine oxidase
  • 2nd gen (SSRIs, SNRIs, NRIs)
  • Tetracyclic (on NA and 5-HT)
  • Melatonergic sleep (MT1, MT2 Agonist, 5HT2c Antagonist)
  • Atypical antidepressants (SERT inhibitor, 5HT receptor modulator)
  • Psychedelics (ketamine = NDMA antagonist, psilocybin; 5-HT2A agonist)
  • St John’s Wort
  • Exercise
17
Q

What do Selective Re-uptake Inhibitors do?

A

These focus the re-uptake of serotonin or noradrenaline or both

18
Q

What are the Selective Re-uptake Inhibitors? and how many are there?

A
  • Selective Serotonin Reuptake Inhibitors (SSRI’s)
  • Noradrenaline Reuptake Inhibitors (NRI’s)
  • Serotonin and Noradrenaline Reuptake Inhibitors
    (SNRI’s)
19
Q

What is the benefit of SRI being more selective?

A

More selective = less side effects

20
Q

What is the receptor for dopamine?

A

D1 and D2 receptors

21
Q

What is the receptor for serotonin?

A

5HT1-A

22
Q

What is the receptor for noradrenaline?

A

Aplha and Beta adrenoceptors

23
Q

Does the release of more of each monoamine calm or excite the receptor? and what is each of these called?

A

Dopamine (EPSP) - excite
Noradrenaline (EPSP) - excite
Serotonine (IPSP) - calm

24
Q

What are the transporters called for each of the monoamines?

A

Dopamine - DAT
Noradrenaline - NET
Serotonine - SERT

25
Q

What transporters do TCAs block?

A

NET, SERT and DAT (all of them) hence the Tri

26
Q

What transporters do SSRI’s block?

A

SERTs (Serotonin)

27
Q

What transporters do NRI’s block?

A

NET (noradrenaline)

28
Q

What transporters do SNRI’s block?

A

NET and SERT (Noradrenaline and serotonin)

29
Q

Neurotransmitters in depression?

A
  • < serotonin
  • < noradrenaline
  • < dopamine
30
Q

Issue with tricyclic anti - depressants?

A

They are cardio-toxic - are easy to suicide with - MAOs are also cardio-toxic

Neuropsychopharmacology (8 decks)

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