Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats

Finasteride inhibits the conversion of testosterone to dihydrotestosterone. Because androgen regulates dopaminergic system in the brain, it could be hypothesized that finasteride may inhibit dopaminergic system. The present study therefore investigates the effects of finasteride in adolescent and early developmental rats on dopaminergic system, including contents of dopamine and its metabolites (dihydroxy phenyl acetic acid and homovanillic acid) and tyrosine hydroxylase expressions both at gene and protein levels. Meanwhile, open‐field behaviors of the rats are examined because of the regulatory effect of dopaminergic system on the behaviors.

Open‐field behaviors were evaluated by exploratory and motor behaviors. Dopamine and its metabolites were assayed by liquid chromatography‐mass spectrometry. Tyrosine hydroxylase mRNA and protein expressions were determined by real‐time qRT‐PCR and western blot, respectively.

It was found that in adolescent male rats, administration of finasteride at doses of 25 and 50 mg/kg for 14 days dose dependently inhibited open‐field behaviors, reduced contents of dopamine and its metabolites in frontal cortex, hippocampus, caudate putamen, nucleus accumbens, and down‐regulated tyrosine hydroxylase mRNA and protein expressions in substantia nigra and ventral tegmental area. However, there was no significant change of these parameters in early developmental rats after finasteride treatment.

These results suggest that finasteride inhibits dopaminergic system and open‐field behaviors in adolescent male rats by inhibiting the conversion of testosterone to dihydrotestosterone, and imply finasteride as a potential therapeutic option for neuropsychiatric disorders associated with hyperactivities of dopaminergic system and androgen.

Keywords: adolescence, dopaminergic system, finasteride, open‐field behaviors, rat

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Something maybe interesting for @orthogs given stated interest in feelings of anhedonia and our take. I’ve written this study up a while ago and there’s something in here that could be of mechanistic importance here in both reward circuitry involvement and the reality that there is a high prevalence of PFS developing in young men (see FAERS data on disability associated with use of finasteride, self report and doctors reports by age).

Again I’ve written a lot more on the mechanistic underpinnings i’ll share in time, but this study was particularly interesting Li et al shows a significant interruption of DHT and AR activation on dopamine neurons in the substantia nigra and ventral tegmental area not seen in older or younger rats, leading the author to conclude dopaminergic signaling is interrupted drastically when AR is inhibited during the time T levels are naturally high. Could this spatiotemporal reliance on appropriate androgen signaling, combined with unknown genetic factors, be involved in why this condition is so significantly greater in young men of fertile age?


Interesting to note. So I suppose you’re saying that younger men, with naturally higher levels of Testosterone than older folk are the most affected in this respect when AR is inhibited.

I wonder if this effect continues after cessation of Finasteride, something the study didn’t cover.

PFS (post-finasteride syndrome) can be described as indicative of its effect by inhibiting dopamine in the central nervous system (CNS).

This link is a short review by a Korean doctor who participated in the Abodat Symposium. Dopamine function of the central nervous system suppression, estimated by the pfs that interesting. I’m curious to know the specific source of this.


I do wonder whether Wellbutrin could therefore work to at least partially relieve the impaired receptors by boosting the amount of dopamine in the brain.

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On December 11th, I’m going to the psychiatrist and I’m going to tell him about the pfs. I will also ask him to prescribe a wellbutrin.

Fin did that, fin did this. How many studies of this sort have we shared here? When will a study try to find causal big picture explanations?

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Your guess is as good as mine.

I used to use medikinet 20 mg. It gave me an improved libido and orgasm, but my erection worsened. Probably due to the vascular contraction of the stimulant.

I would like to try cabergoline or bromocyptine. It would have been possible if we had a blood test when Galactorrhea was present. I regret it.

Been taking Wellbutrin for a year and a half and coming off next week. Don’t expect miracles…


I totally agree with you. A small improvement is only an improvement. It is not a fundamental remedy. Our system is completely ruined.

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I have taken Prami as well as Caber and neither benefited in any way.

The one (or few) times that I have had a sexual recovery, I was taking Mucuna Pruriens combined with Tribulus. Mucuna works by increasing dopamine. Over time it stopped working though.

Have you also tried L-phenylalenine, another dopamine precursor?

I guess, if we want to boost dopamine, then we really have to pull some big weapons like research chemicals… 9-Methyl-β-carbolin would be my number one chemical to try, but again im waiting the 1 year mark. Stalemate is not an option…Not in my dictionary at least…Its either 100% recovery, or death…


Good luck to you. Would 95% suffice?

I think there was a prolactin increase caused by finasteride because there was galactorrhea. Dopamine is a major inhibitor of prolactin. But dopamine agents are of no use to us. It’s a completely unknown area. Damn it, Merck! They shouldn’t sell this stuff.

I took Welbutrin for a long time and it had no sexual benefit, only a very mild AD effect at the expense of IQ — its anti-cholinergic effects made me stupid.

An interesting dopamine drug is Modafinil. I haven’t taken it in ages so don’t know the sexual effects, but it definitely elevated my mood and did not seem to increase anxiety or make me feel drugged/wired like other stimulants do.

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