Affective Disorders Flashcards

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1
Q

How do Monoamine Oxidase Inhibitors [Iproniazid] work?

A

Inside axonal ending, destroys MAO so it can’t destroy neurotransmitters - agonistic. Very small error margin [danerous]

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2
Q

How do reuptake inhibitors work?

A

Increase transmitter substance in synaptic cleft [agonist]

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3
Q

What are common reuptake inhibitors?

A

tricyclics [work with dopamine, seratonin, norepinephrine]
SSRI - seratonin [Prozac]
SNRI - seratonin &/or norepinephrine inhibitors

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4
Q

What is ketamine?

A

NMDA antagonist [reduces glutamate transmission]

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5
Q

What is the primary neurotransmitter?

A

acetylcholine

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6
Q

What is the enzyme that destroys acetylcholine?

A

acetylcholinesterase

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7
Q

What do MAO inhibitors inactivate?

A

Acetylcholinesterase [agonistic]

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8
Q

What does cocaine do?

A

Inhibit reuptake of dopamine [agonist]

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9
Q

What does ketamine do, long term?

A

produce schizophrenia-like symptoms

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10
Q

What are brain stimulation techniques used for depression?

A

ECT, TMS, deep brain stimulation of subgenual anterior cingulate cortex, stimulate vagus nerve

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11
Q

Why is vagus nerve important?

A

descends into PNS - stimulation reduces depressive effects

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12
Q

What is monoamine hypothesis of depression?

A

Depression results from reduced activity of brain monoamines

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13
Q

What is evidence for monoamine hypothesis of depression?

A

Reserpine prevents storage of NT in vescicles –> depletion of monoamines –> depression
Suicidal depression related to low level of 5-HIAA [metabolised seratonin]
Antidepressants increase NE or 5-HT [by blocking monoamine reuptake]
Tryptophan deletion procedure - reduces 5-HT levels, reinstates depression in former depressed patients

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14
Q

What is tryptophan?

A

precursor to seratonin

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15
Q

What were effects of tryptophan depletion [lowering brain serotonin] and catecholamine depletion on symptoms of patients receiving SSRI or NERI [norepinephrine reuptake inhibitor?

A

SSRI patients relapsed when serotonin depleted; NERI patients relapsed when catecholamine depleted
Therefore two types of depression patients

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16
Q

What are problems with monoamine depletion theory?

A

Antidepressant meds take two weeks to work

Depletion procedure only has depressant effect in people with personal or family history [those with risk factors]

17
Q

What is tentative evidence for brain abnormalities?

A
  • decreased levelts of neurotrophic factor
  • enlarged ventricles; decreased hippocampal volume
  • high levels of activity in amygdala and medial orbital prefrontal cortex
  • high levels of activity in subgenual ACC; decreased activity in other frontal areas
  • silent cerebral infarctions
18
Q

What is the 5-HT transporter

A

reuptake mechanism for serotonin

19
Q

What does short allele in 5-HT transporter gene indicate?

A

pathological; impairs re-uptake, increasing availability of serotonin in the synapse

20
Q

What does possession of one or two short alleles predispose to?

A

depression

21
Q

How might short alleles predispose to depression?

A

influences over prenatal development, esp in amygdala and subgenual ACC

22
Q

What do REM sleep patterns in depressed patients show?

A

Longer REM periods earlier in night

Don’t get slow wave sleep

23
Q

What does REM deprivation do?

A

Improve mood

24
Q

What do antidepressants do to REM sleep?

A

Suppress it, increase slow wave sleep

25
Q

What is effect of short REM sleep latency?

A

increases chance of depression

26
Q

What is effect of living in total darkness on monoaminergic systems?

A

decreases number of terminal buttons from DA neurons, NE neurons and 5-HT neurons