Some atypical antipsychotics are used in addition to antidepressants to treat episodes of severe depression, at a lower dosage than those that induce an antipsychotic effect.
But what mechanism underlies the antidepressant effect of the atypical antiipsychotics: The 5HT2C antagonism ?
I agree that it is probably about 5-HT2C antagonism, but not only. Although antagonism at 5-HT2A receptors enhances the release of dopamine into the prefrontal cortex, 5-HT2C antagonism alone is obviously sufficient for an antidepressant action, for example in the case of relatively new antidepressant agomelatine. 5-HT1A agonism is associated with anxiolytic and antidepressant effects, for example in clozapine or aripiprazole. However, some antipsychotics, such as ziprasidone, also inhibit the reuptake of noradrenaline and serotonin. There are many neuropsychopharmacological effects of antipsychotics that mediate their antidepressant action and it is not quite a clear matter yet.
Thank you Patarak for your reply. In addition, I also saw that amisulpride is a 5HT7 antagonist,as the recent andidepressant vortioxetine...
I always forget to take in account this 5HT1A agonism...: shouldn't we expect,in addition to the activation of the post synaptic 5HT1a, an activation of the 5HT1a at the somatodendridic level of the serotoninergic neurons, that may lead to a decrease of release of 5HT. It may have a pro depressant effect until a probable desensitization? Do you know what is the range of affinity for this 5HT1a? Is it as strong as the 5HT2C?
Thank you also Peng for your reply. Excuse me, but I am wondering if there is not a mistunderstanding: I wanted to ask about the antidepressant effect of the atypical antipsychotics. Not the antipsychotic effect by itself :)
(Indeed, for example, you mentioned the D2. Is it not admitted that blocking the D2 receptors induces, on the contrary, a depressiogenic effect? )
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