Interesting facts here, namely the “medial preoptic area” (MPOA) and it’s need for dopamine and nitric oxide synthase to function and effectively induce sexual behavior. While not ultra-revealing, the biggest aspect here is that the gonad-having group had more extracellular (usable I presume) DA. Hence T metabolites, and they name DIHYDROTESTOSTERONE here, stimulate the activity of DA in this region of the brain. Meaning that if you want this brain section to do its job and activate sexual behavior, you’d better have DHT around to promote DA release.
Furthermore, T is also cited as upregulating neuronal Nitric Oxide Synthase, which is another significant neurochemical in signaling this brain area’s DA.
Note: “Medial preoptic nucleus releases gonadotropin-releasing hormone.” - Wikipedia. As Nitric Oxide helps stimulate the release of GnRH, it follows that without NOS, this is another source of GnRH muted when deprived of androgen, hence downregulating the HPTA function.
Thanks Propecia! Yet another significant biomechanism disrupted. 
[Size=4]Effects of testosterone metabolites on copulation, medial preoptic dopamine, and NOS-immunoreactivity in castrated male rats [/size] [Size=4]
Susan K. Putnam1, Satoru Sato, Jon V. Riolo and Elaine M. HullCorresponding Author Contact Information, E-mail The Corresponding Author
Department of Psychology, State University of New York at Buffalo, Buffalo, NY 14260-4110, USA[/size]
The medial preoptic area (MPOA) is an important integrative site for male sexual behavior. Dopamine (DA) is released in the MPOA of male rats shortly before and during copulation. In a previous study, we identified 17β-estradiol (E2) as the metabolite of testosterone (T) that maintains MPOA basal extracellular DA levels. However, the presence of dihydrotestosterone (DHT), an androgenic metabolite of T, is required for the female-induced increase in MPOA DA observed during copulation. Recently, we reported that assays of MPOA tissue DA content showed that castrates actually had more stored DA than did gonadally intact males. Therefore, the reduction in extracellular levels in castrates was not due to decreased availability of DA; most likely it was due to decreased release. Furthermore, [b]T upregulates neuronal nitric oxide synthase (nNOS) in the MPOA. NO has been implicated in the regulation of DA release in the MPOA.[/b] It is not known, however, which metabolite(s) of T regulate(s) tissue stores of DA and/or nNOS in the MPOA of male rats.
The present experiments were designed to test the following: (1) whether E2, DHT, or the combination of the two influences MPOA DA tissue levels, an indication of stored DA, in male rat castrates; and (2) whether E2, DHT, or the combination of the two influences NOS-ir in the MPOA of castrated male rats.
The results indicate that E2 up-regulates nNOS-ir in the MPOA and maintains tissue content of DA at levels similar to those in T-treated rats. DHT did not influence nNOS-ir, while attenuating the effect of castration on tissue DA content.