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Abilify (aripiprazole) is approved by the FDA for augmentation to antidepressants that have not been effect patients, therefore treatment resistant. It is also the only indicated atypical antipsychotic. It is peerless in the fact that it has dopaminergic partial agonism, but what are its primary serotonergic mechanisms? Antagonism at the 5-HT2A receptor (Ki = 8.7 nM), and partial agonism at the 5-HT1A receptor (Ki= 5.6 nM), 5-HT7 receptor (Ki = 10 nM), 5-HT2C receptor (Ki = 22.4 nM) Latuda is indicated for bipolar depression, however. What serotonergic actions does lurasidone have? Antagonism at the 5-HT2A receptor (Ki = 2.0 nM), 5-HT7 receptor (Ki = 0.5 nM), 5HT2C receptor (Ki = 415 nM) and partial agonism at the 5-HT1A receptor (Ki = 6.8 nM). According to Wikipedia (disclaimer: I am the author): Aripiprazole's primary serotonergic effect is at the 5-HT2B receptor where it functions as an antagonist with a Ki of 0.36 nM. Trazodone antagonizes the 5-HT2B (Ki = 78.4 nM) stronger than any serotonergic receptor except for 5-HT2A (Ki = 8.7 nM). Also, there are six 5-HT receptors that trazodone and aripiprazole both effect, but their strength varies in order. Aripiprazole's order of strength is as follows: 5-HT2B receptor, 5-HT1A receptor, 5-HT7 receptor, 5-HT2A receptor, 5-HT2C receptor, 5-HT1D receptor. Trazodone's order of strength is as follows: 5-HT2A receptor, 5-HT2B receptor, 5-HT1D receptor, 5-HT1A receptor, 5-HT2C receptor, 5-HT7 receptor. Trazodone has strong similarities to the atypical antipsychotic, aripiprazole, and both psychiatric medications produce the mCPP metabolite. With Abilify and Latuda, the mutual serotonergic receptors are as follows: 5-HT2A, 5-HT7, 5HT2C, and 5-HT1A. Abilify is nonpareil because it has partial agonism properties comparatively to the other atypical antipsychotics. Also, you cant discount the fact that trazodone possesses 5-HT2A/2C antagonism. 5-HT2A/2C antagonists could mediate antidepressant effects by elevating the levels of dopamine and norepinephrine in the prefrontal cortex. 5-HT2A/2C antagonism intensification to SSRI/SNRI action may potentiate the antidepressant effects in treatment resistant patients. Atypical antipsychotics, which have 5-HT2A antagonist effects as prominent properties, are proven to potentiate the actions of SSRIs/SNRIs (see Abilify) in these patients. There are several agents with 5-HT2C antagonist actions that are currently on the market approved as antidepressants. Dopamine is not a factor of the depression hypothesis rather serotonin is indicated as the primary factor of depression, and I believe that Abilifys strong antidepressant effects are exerted by its serotonergic action which could also be mediated via trazodone. SERT inhibitors, such as SSRIs and SNRIs, raise every serotonin receptor all at once and simultaneously cause antidepressant action by stimulating the 5-HT1A receptors, but they cause Nolan