Affective Disorders Flashcards

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
What is effect of short REM sleep latency?
increases chance of depression
26
What is effect of living in total darkness on monoaminergic systems?
decreases number of terminal buttons from DA neurons, NE neurons and 5-HT neurons