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PMCOL 200 > Depression > Flashcards

Depression Flashcards

1
Q

what is depression?

A

recurring or debilitating mental disorder that impairs social and/or occupational functioning (most common mood disorder)

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2
Q

what neuronal system are emotions vs motivations part of?

A

emotions: limbic system
motivations: mesocorticolimbic system

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3
Q

what is the limbic brain?

A

cortical border circling the brainstem (oldest part of cortex)

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4
Q

what 4 brain structures are a part of the limbic brain?

A

amygdala, hippocampus, basal ganglia, and cingulate gyrus (also connects to frontal cortex and hypothalamus)

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5
Q

MDD is associated w/ incr activity in ______ regions and decr activity in the ________

A

incr in limbic (amygdala)

decr in striatum (motivation)

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6
Q

NTs in what region may be responsible for depression?

A

limbic

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7
Q

what are 3 monoaminergic NTs?

A

dopamine, norepinephrine, and serotonin

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8
Q

what do alterations in monoaminergic NTs cause and why?

A

mood disorders; regulate mood, arousal, and attention

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9
Q

what is the amine hypothesis of depression?

A

depression results from inadequate monoamine neurotransmission (serotonin and noradrenaline)

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10
Q

what could cause decr monoamine neurotransmission?

A

less NT release, fewer receptors, impaired signal transduction

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11
Q

what were long-term effects of reserpine?

A

15% of patients developed depression-like syndrome

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12
Q

how does reserpine cause depressive symptoms?

A

depletes neurons of dopamine and norepinephrine (inhibits presynaptic NT uptake into vesicles and decr release)

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13
Q

what is ipronazid?

A

anti-tubercular drug that alleviated depression

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14
Q

how did ipronazid alleviate depression?

A

inhibited monoamine oxidase/MAO (enzyme that breaks down monoamine NTs) which incr [monoamine NTs]

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15
Q

what are 3 issues w/ monoamine hypothesis for depression?

A

drugs that restore monoamine levels are moderately effective in 30-50% of patients; inconclusive evidence 5-HT and NA are disrupted in depression; antidepressants take weeks for clinical effects (NT levels change immediately)

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16
Q

what is the glutamatergic hypothesis?

A

depression is associated w/ decr glutamatergic signaling in cortex

17
Q

what does decr in glutamatergic signalling impact?

A

both excitatory and inhibitory function, leading to reduced signal noise

18
Q

what does loss of glutamatergic signalling also cause? (4)

A

long-term potentiation, neurotropic production (BDNF), synapse formation, gene transcription

19
Q

what do MAO inhibitors do?

A

incr synaptic levels of monoamine NTs (NE and 5-HT) by inhibiting their breakdown by MAO

20
Q

what is an example of an MAO inhibitor?

A

ipronazid

21
Q

what is the “tyramine cheese rxn”?

A

inhibition of MAO by MAO inhibitors can incr [tyramine] and cause acute hypertension (binds to adrenergic receptors in heart and blood vessels)

22
Q

what is tyramine?

A

sympathomimetic monoamine (resembles NA) found in foods such as aged cheese

23
Q

what is tyramine degraded by?

A

MAO

24
Q

what does SSRI stand for?

A

selective serotonin reuptake inhibitors

25
Q

what do SSRIs do?

A

inhibit serotonin (SET) transporters which incr extracellular [5-HT]

26
Q

what are transporters?

A

molecules that reuptake NTs from synapse into cell

27
Q

what does SNRI stand for?

A

serotonin norepinephrine reuptake inhibitors

28
Q

what do SNRIs do?

A

inhibit SETs and NA transporters (NETs)

29
Q

what is an example of a selective reuptake inhibitor?

A

fluoxetine

30
Q

what are 3 limitations of monoamine antidepressants? (MAOIs, SSRIs, SNRIs)

A

only moderately effective in 30-50% of patients; take several weeks for clinical effect (immediate effects on NT levels); on-target side effects such as nausea, indigestion, dizziness, dry mouth, weight loss, etc.

31
Q

what is ketamine?

A

a noncompetitive NMDA/Glu receptor antagonist

32
Q

what are 3 purposes for ketamine?

A

anti-depressant (low doses), hallucinogen (medium doses), dissociative anesthetic (high doses) - lethal at higher doses

33
Q

how does ketamine work to improve symptoms of depression?

A

blocks activation of NMDA receptors on GABAergic interneurons by Glu which inhibits inhibition (activates) Glu excitatory neurons (incr [Glu])

34
Q

what are 4 downstream effects of Glu burst from ketamine?

A

synaptic remodeling, resetting of Glu and GABA systems, BDNF release, gene transcription

35
Q

what is the effectiveness of SSRIs vs ketamine?

A

SSRIs: ~15% in 8 weeks
ketamine: ~25% in one day

36
Q

what are 2 limitations of ketamine?

A

narrow TI; must be administered intravenously in hospital (due to small TI)

37
Q

what are future/possible treatments for depression?

A

drugs that directly target downstream events from synaptic remodeling (inositol, cAMP, CREB) to be more effective and selective

38
Q

what is rolipram?

A

phosphodiesterase inhibitor that incr cAMP to treat depression

PMCOL 200 (27 decks)

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