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Exact-Swan-3136 t1_iv6joaz wrote

I am trying to understand the mechanism of this experiment. They dosed rats with a dopaminergic substance (amphetamines), and then cut off half of them (to cause depression), and then they measured the differences in serotonin in each group? This would suggest serotonin deficiency is symptomatic. Was there a control group measured without any amping at all? Which brings me to my next question, could dopamine then reverse the depression? Instead of serotonin?

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LysergioXandex t1_iv7q46r wrote

I’ve only read the abstract.

First, this experiment was done in human patients (17 depressed, 20 healthy controls).
They give the amphetamine not to induce “depression” but to simulate dopaminergic stimulation, which activates serotonin-releasing neurons downstream.

They also administer a radioactive ligand for the serotonin 5-HT2a receptor, which is one of the “targets” of released serotonin. By measuring how much radioactivity is displaced after the amphetamine-induced serotonin flood, they can measure approximately how much serotonin must have been released.

I’m not in this field, but some questions this study raises for me include:

  • does depression alter the activity of amphetamine.
  • are 5HT2a receptors and Dopamine Transporters (amphetamine target) differently expressed in depression.
  • are the inhibitory autoreceptors for serotonin (eg 5HT1 a/b/d) expressed in different proportion to 5HT2a receptors in depression?
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