Update:
I have received an email from Georgi about why it increases serotonin:
Pramipexole is actually known to the Peat community and Peat was asked about pramipexole several times, and he cautioned against using it. It seems that this drug desensitizes the 5-HT1A receptor, which is a so-called "autoreceptor" and its activation decreases firing of 5-HT neurons and overall 5-HT tone in the brain. So, a desensitized 5-HT1A would mean increased serotonin tone/release and thus firing of the 5-HT neurons. This may be one reason Peat cautioned against using it. It also has several unpleasant side effects such as increased compulsive sexual behavior, which medicine claims is due to dopamine overload, but recent studies have shown that the culprit is serotonin. So, pramipexole seems to have a strong serotonergic effect in addition to its dopamine agonism, which seems to be missing in other dopamine agonists such as bromocriptine and the rest of the ergot derivatives.
https://haidut.me/?p=2895
https://pmc.ncbi.nlm.nih.gov/articles/PMC3297071/
"...The hippocampus and prefrontal cortex (PFC), structures manifesting volume decreases in depressed individuals, are also affected in rodents with chronic stress.20–24 It is not surprising that one of the common pathways for antidepressant response is an increase in the gene expression of neurotrophic/neuroprotective factors in the PFC and hippocampus.25,26 Previous work documented that prolonged administration of PPX in rats induced a desensitization of somatodendritic D2 autoreceptors in the ventral tegmental area (VTA), allowing the firing of DA neurons to normalize, and of 5-HT1A receptors in the dorsal raphe (DR) that enabled the spontaneous firing rate of 5-HT neurons to increase above control levels.27 Considering the effectiveness of PPX in the treatment of MDD, the importance of both DA and 5-HT systems in the pathophysiology of depression, and the DA innervation of the PFC and the 5-HT innervation of the hippocampus, the assessment of the net effect of chronic PPX administration on DA and 5-HT neuronal tone in the PFC and hippocampus, respectively, was deemed relevant to understand its antidepressant action."
"...Similarly to PPX, the increase in the spontaneous discharge of DR 5-HT neurons produced by subchronic administration of the atypical antipsychotic aripiprazole has been found to be due to activation of the D2-like receptors and desensitization of 5-HT1A autoreceptors.62 "
Let's see what happens with a microdose.
