Some simple googling turned this up:
jop.sagepub.com/cgi/content/abstract/10/4/266
“Allopregnanolone reduced (by a maximum of 65 to 75%) basal dopamine content in the prefrontal cortex and nucleus accumbens in a dose-dependent manner, but had no effect on dopamine output in the striatum.”
“These results suggest that endogenous neurosteroids may participate in the GABAergic modulation of dopaminergic transmission in the rat cerebral cortex and nucleus accumbens, two brain areas which are important in the regulation of emotional processes.”
In the paradigm of the rat, allopregnanolone actually reduces dopamine (implying that the effect of fin would be to increase dopamine). Obviously, since this study involves rats, no substantial conclusions about human allopregnanolone functions can be drawn.
However, if we want to assume that this is a perfect model, we might be able to conjecture that decreased allopregnanolone does cause an increase in dopamine, which in turn acts upon other mechanisms that work to downregulate dopamine production. Maybe the activity of these downregulatory mechanisms persists even after allopregnanolone returns to normal, thus explaining statis dopamine levels that are lower than originally.
Personally I’m starting to come around to the progesterone cream idea. Better still would be synthetic allopregnanolone.
Keep in mind too that women who are continually cycling experience frequent allopregnanolone deficiency as well (aka PMS), and could maybe serve as a model.
The fin-induced deficency of course is much longer than 5 days/month however, and could maybe lead to more significant effects throughout the brain?
Nevertheless, even if this were the case, and I’ve said this several times before, I would be very hard pressed to advocate a ‘replacement’ solution, like that pursued by letsconvenience. These treat symtoms not causes.
As for the neurotransmitter issue, therefore, whatever the mechanism may be (and we may very well never know), it would seem that a very simple sort of logic might produce results. Knowing there is a state of dysfunction within the brain, and also knowing the cause of that dysfunction (fin-induced decrease in allopregnanolone / increase in progesterone), and also maybe throwing in some intuitively-appealing assumptions (i.e. that it probably required prolonged exposure to this imbalance in order for widespread dysfunction to ultimately take place), I think we come to one simple solution for the problem - reversing the initial imbalance and holding it there for a period of time.
Progesterone cream, obviously, would not be a perfect candidate as we do not need to increase progesterone concentrations.
The only thing that comes to mind really is alcohol, which, in contrast to inhibiting brain 5AR as fin does, actually acts to stimulate it. Alcohol consumption should thus tilt the balance toward lower progesterone and higher allopregnanolone. But alcohol has other effects as well, which may act to complicate this solution.
Ideally, it would seem, you’d want to find a brain 5AR stimulator that has an absolute minimum of peripheral effects. Or maybe progesterone cream would work, and the elevated progesterone would have an insignificant effect, as maybe it was the allopregnanolone deficiency that had the most negative effect?
