Monoamine hypothesis

Question 1

Several findings indicate

Answer 1

Decreased serotonin and norepinephrine are involved in depression

Question 2

Even though dopamine is a monoamine, dopamine agonists such as cocaine and amphetamine do not

Answer 2

Improve depression, indicating serotonin and norepinephrine are the monoamines involved

Question 3

Monoamine antagonists cause depression

Answer 3

Reserpine monoamine inhibitor used to treat HTN and caused depression

Question 4

Tryptophan depletion

Answer 4

1. eat low tryptophan diet first day and drink amino acid cocktail without tryptophan the next
   - “drastically reduces” brain levels of tryptophan  precursor to serotonin
2. depressed patient taking meds and “feeling well” relapsed with tryptophan depletion and recovered when eating normal diet
3. tryptophan depletion has no effect on mood of healthy normals, but lowers mood in people with family history of affective disorder
4. tryptophan depletion causes relapses in patients successfully treated with SSRI but not patients effectively treated with NE reuptake inhibitors
5. AMPT - which inhibits synthesis of DA and NE - causes relapse in patients treated with NE reuptake inhibitors but does not in patients taking SSRI
6. PET showed patients who relapsed on tryptophan depletion had decreased activation of prefrontal lobe

Question 5

Although evidence indicates 5HT and NE play important role in depression, monoamine insufficiency likely is not the only or primary causative factor

Answer 5

is not the only or primary causative factor:

1. SSRI and SNRI rapidly increase levels of 5-HT and NE in brain but do not relieve sxs of depression for weeks
2. And decreasing 5HT levels in brains of people with no family hx of depression does not affect mood
3. Increased extracellular levels of 5-HT and NE likely start a chain of events that eventually produce decrease in depression, but this chain is not known