Interesting stuff I came across. I remember in a Bostin Lloyd video he says prami helps keep him sane during a tren cycle. See, you guys are missing out if your not taking anti-prolactin measures. Found these two studies. Tell me what you guys think.

Prami:

Major Depression In (PMID 10812530), (PMID 12479663), (PMID 15219473), and (PMID 14992985) pramipexole was tested as a lone antidepressant (first study), as an adjunct to an antidepressant (second study), or as an adjunct to a mood stabilizer (third and fourth studies). In all four, it showed considerable efficacy in major depression or bipolar depression. The first is probably most interesting, as it showed (relatively) high-dose pramipexole alone may be as effective as fluoxetine in the treatment of MDD.

Synergy With SSRIs In (PMID 16963794), data suggests that not only is pramipexole effective as an antidepressant, but it may actually synergize with SSRIs (at least setraline and fluoxetine) in a fairly interesting way. (See the study for details.)

Mechanism The study (PMID 18688211), though in rats, is probably the most interesting I've found. I'm going to simply quote the last portion of the abstract:

After 14 days of PPX treatment, the firing rate of DA had recovered as well as that of NE, whereas the firing rate of 5-HT neurons was increased by 38%. It was also observed that sustained PPX administration produced desensitization of D(2)/D(3) and 5-HT(1A) cell body autoreceptors, as well as a decrease in sensitivity of alpha(2)-adrenergic cell body autoreceptors. These adaptive changes are implicated in long-term firing rate adaptations of DA, NE and 5-HT neurons after prolonged PPX administration. In conclusion, the therapeutic action of PPX in depression might be attributed to increased DA and 5-HT neurotransmission.

In short, though pramipexole is a D2/D3 agonist, it rather dramatically increased the firing rate of 5-HT neurons and desensitized 5-HT(1A) and D2/D3 autoreceptors. The implication is that it should, with chronic use, improve D2 and 5-HT1A sensitivity and increase 5-HT neurotransmission. As all three of these factors have been implicated in major depression (among other psychiatric disorders), this seems absolutely enormous. And note that this study is from 2009, so it's implications have not yet filtered out.

Antidepressant effects of pramipexole, a novel dopamine receptor agonist.
Maj J, Rogóz Z, Skuza G, Kołodziejczyk K.
Source
Institute of Pharmacology, Polish Academy of Sciences, Kraków.
Abstract
Pramipexole (2-amino-4,5,6,7-tetrahydro-6-propyl-amino-benzthiazole-dihydrochl oride), a new dopamine receptor agonist with preference for D3 compared to D2 and D4 receptors, was tested in rats in respect of its potential antidepressant activity. In the forced swimming test the drug under study, given three times in rats, reduced the immobility time. In the forced swimming test, joint treatment with antidepressants (imipramine, amitriptyline) and pramipexole evoked a more potent effect than any of the drugs given alone; however, the locomotor hyperactivity was weaker after joint administration. Citalopram and fluoxetine, inactive per se in the forced swimming tests, visibly enhanced the antidepressant-like effect of pramipexole but, on the other hand, they attenuated the locomotor hyperactivity evoked by the drug. Repeated treatment with pramipexole (0.3 or 1 mg/kg, twice daily for 14 days) increased the locomotor activity measured at 1 h after the last dose. Repeated administration of pramipexole (as above) potentiated the D-amphetamine- or quinpirole-induced locomotor hyperactivity. The obtained results indicate that, in the tests used, pramipexole evokes effects similar to those of typical antidepressants and, at the same time, enhances their activity (the forced swimming test in rats); therefore it may be regarded as a potential antidepressant drug.

Caber:

Cabergoline, a dopamine receptor agonist, has an antidepressant-like property and enhances brain-derived neurotrophic factor signaling.
Chiba S, Numakawa T, Ninomiya M, Yoon HS, Kunugi H.
Source
Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashi, Kodaira, Tokyo 187-8502, Japan.
Abstract
RATIONALE:
Dopamine agonists have been implicated in the treatment of depression. Cabergoline is an ergot derivative with a high affinity to dopamine D(2)-like receptors; however, there have been few preclinical studies on its antidepressant-like effects.
MATERIALS AND METHODS:
Behavioral effects of cabergoline were examined in rats using forced swimming (FST), novelty-suppressed feeding (NST), open field (OFT), and elevated-plus maze (EPT) tests. In a single treatment paradigm, behaviors of rats were analyzed 4 h after single injection of cabergoline (s.c., 0-4 micromol/kg). In a repeated-treatment paradigm, OFT, EPT, and FST were conducted on days 11, 12, and 13-14, respectively, during daily cabergoline injections (s.c., 0.5 micromol/kg), and then hippocampus was removed 24 h after the last injection. NST was conducted in a separate experiment at day 14. Western blotting was used for the analysis of the protein levels of brain-derived neurotrophic factor (BDNF) and the activation of intracellular signaling molecules.
RESULTS:
Single injection of cabergoline demonstrated decreased immobility in FST and distance traveled during 0-10 min in OFT, while time spent and entry into open arms were increased at 4 micromol/kg. When cabergoline was repeatedly administered, immobility in FST and the latency of feeding in NSF were significantly reduced, while vertical movement was increased in OFT. The time in closed arms was tended to be decreased in EPT. Expression of BDNF and activation of extracellular signal-regulated kinase 1 were up-regulated after the chronic administration of cabergoline.
CONCLUSIONS:
Cabergoline exerts antidepressant- and anxiolytic-like effects, which may be mediated by potentiation of intracellular signaling of BDNF.

http://www.ncbi.nlm.nih.gov/pubmed/20526584
http://www.ncbi.nlm.nih.gov/pubmed/9295183