Lecture 20.docx - DEPRESSION OVERVIEW[see image[see image...

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DEPRESSION: OVERVIEW [see image] [see image] - Depression is thought to be due to decreases in catecholamines and serotonin o There are actually two dueling hypotheses: o Catecholamine Hypothesis: Depression is somewhat related to the amygdala as well as the reticular formation – low levels of norepinephrine, dopamine, (and epinephrine?) signaling (alertness, wakefulness – depression often involves lethargy and hypersomnia) Evidence: giving reserpine (blocks loading of catecholamines/norepinephrine into vesicles) can mimic depression symptoms long-term o Serotonin Hypothesis: Depression is related to serotonergic functioning (think of SSRIs – antidepressant which blocks serotonin transporters so it’s not reuptake into axon terminal similar to MDMA function – but also causes increase vesicular release and remove serotonin from vesicles. SSRIs result in a slow, gradual build up of serotonin in synapse - so-much-stronger-than-the-difference-between-Ritalin-and-Adderall SSRI allow serotonin levels to slow rise over a few days/weeks Some depressed patients have reduced serotonergic functioning, along with increased serotonin catabolism/metabolism – serotonin being broken down more quickly less available serotonin less being reuptake each release neuron starts falling behind and has to produce more to keep up
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Greater turnover means less available serotonin TREATING DEPRESSION - We tried to use stimulants but it didn’t work o Dopamine levels didn’t help person during acute effects. Withdrawal from decreased levels would make depression symptoms worse (clue for catecholamine hypothesis) - MAOIs: same compound in tobacco o Inhibit monoamine oxidase less breakdown of DA, NE, and 5-HT increased levels of monoamine (DA, serotonin, epinephrine) o But same concerns from MAOIS from tobacco - Cyclics: o Tricyclics: amitriptyline and imipramine Comes from their structure, three organic chemistry rings w side arms Work by blocking serotonin and NE (5HT receptor) reuptake (nonselective) To a much lesser extent, also block DAT Dirty compounds: have been shown to act on NE receptors, NMDA receptors (glutamate), certain 5-HT receptors, and histamine o Heterocyclic: classic SSRIs, more selective than tricyclics and zone in on serotonin specifically. Not everyone responds because not everyone’s depression is from low serotonin Fluoxetine (Prozac), Paroxetine (Pacil), Sertraline (Zoloft) - Tricyclics and MAOIs were discovered by accident o Tricyclics were being investigated as antipsychotic medications o MAOIS were used for TB Helped with anhedonia patients for TB patients o Caveat: cellular changes happen within hours, but the behavioral effects take weeks This length process contributes to individual’s malaise of figuring out what will work - Side effects: o Tricyclics: since they’re dirty/non-selective Drowsiness (histamine receptors)
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  • Fall '19
  • Selective serotonin reuptake inhibitor, Antidepressant, Benzodiazepine, BZDs

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