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Quantitative autoradiography was used to investigate the distribution and effects of gonadal hormones on [3H] muscimol (specific GABAA receptor ligand) binding in the male Japanese quail brain. In gonadally intact Japanese quail brains, [3H] muscimol revealed a heterogeneous distribution with high GABAA receptor levels in the cerebellum pars granularis (656 fmol/mg wet weight of tissue) and in the pars molecularis (405 fmol/mg wet weight of tissue). Low receptor levels were found in the nucleus preopticus anterior and the nucleus lateralis of the hypothalamic regions (less than 220 fmol/mg wet weight of tissue) as well as thalamic nuclei such as rotundus and pretectalis (220-261 fmol/mg wet weight of tissue). Castration resulted in [3H] muscimol binding changes in both brain areas that contain steroid receptors and brain areas devoid of steroid receptors. In fact, castration led to high binding levels in the preopticus anterior nucleus and in the anterior neostriatum area, brain areas that are known to contain gonadal steroid receptors. Castration also elevated [3H] muscimol binding in the hyperstriatum ventrale and reduced binding levels in the paleostriatum augmentatum and the stratum griscum centrale area; all of these areas are known to be devoid of gonadal steroid receptors. At this point it was also important to know whether the gonadal steroid effect is due to alterations in the number of binding sites (Bmax) and/or the affinity binding state (KD). The saturation binding study, dealing with some of the areas described above in brains of male quails castrated or castrated and treated with testosterone or estradiol, demonstrated that the steroid replacement therapy was responsible for the changes of the Bmax.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative receptor autoradiography was used to study the neuroanatomical distribution and effects of gonadal hormones on [³H] flunitrazepam binding in the male Japanese quail brain. In gonadally intact quail brains, [³H] flunitrazepam displayed a heterogeneous distribution, with elevated levels in the posterior brain regions such as the stratum griseum et fibrosum superficiale and stratum griseum centrale of the optic tectum. Lower values were observed in the anteriorly located brain sites such as the nucleus septalis (lateralis et medialis), the cortex dorsolateralis and the nucleus lateralis hypothalami. Castration affected [³H] flunitrazepam binding levels in brain areas known to contain gonadal steroid receptors as well as in some areas which were devoid of gonadal steroid receptors. Castration in fact, elevated [³H] flunitrazepam binding in the nucleus preopticus anterior and reduced binding levels in archistriatum dorsalis et ventralis and in the nucleus intercollicularis; all of these areas are known to have gonadal steroid receptors. In two regions which do not contain such receptors, namely the hyperstriatum ventrale and the cerebellum pars granularis, castration increased [³H] flunitrazepam binding. In order to determine whether the gonadal steroid effect is due to changes either in the number of binding sites (B_max) and or affinity binding state (KD), saturation binding studies were carried out in some of the areas described above in brains of quail which were castrated or castrated and given replacement therapy with testosterone or estradiol for 2 weeks. In keeping with the suppressive effect of the gonads inferred from the castration results described above, testosterone and estradiol decreased the B_max of [³H] flunitrazepam binding in the hypothalamus preoptic area, while in hyperstriatum ventrale only estradiol produced a significant decrease of the B_max. We then tested for the effects of GAB A on [³H] flunitrazepam binding to the receptors and found that GABA intensified the depressive activity of gonadal steroid replacement therapy in the hyperstriatum ventrale and in the hypothalamus-preoptic area as shown respectively by the approximate 45 and 40% greater decrease of B_max. However when the GABA effect on [³H] flunitrazepam binding in the presence of GABA was expressed as ratio, only the hyperstriatum ventrale revealed a significantly enhanced potentiation effect following castration, while a significant suppression of this potentiation effect was obtained by both T and E replacement therapy. These results suggest that a GABA-benzodiazepine receptor interaction might be involved in the regulation of some hormone-mediated cerebral functions in the male quail such as neuroendocrine and sociosexual behavior.

The adrenal gland of castrated adult male rats metabolized [3H]dehydroepiandrosterone in vitro to delta 4-androsten-3,17-dione (4AD), testosterone, dihydrotestosterone (DHT) and 5 alpha-androstane-3,17-dione (5 alpha AD). Despite the low testosterone values, DHT and 5 alpha AD were higher 30 and especially 60 days after castration, with raised 4AD:testosterone and decreased testosterone:DHT ratios. The 5 alpha-reductase activity thus appears to increase with time after castration. Fourteen days after castration, 4AD was the only metabolite that was raised compared with intact animals, and testosterone was comparable in sham-operated and castrated rats. The administration of testosterone propionate to castrated rats restored testosterone values to those of intact rat adrenals, whereas 4AD values were greater. The administration of dihydrotestosterone propionate also yielded higher levels of 4AD, in the presence of a lower testosterone value. After administration of oestradiol benzoate, 4AD values were lower especially compared with the other hormone-treated groups, and there was an unexpectedly high testosterone value. These data indicate that the adrenal gland contributes to the production of androgens, as previously noted by Andò, Canonaco, Beraldi et al. (1988) who showed increased plasma 4AD and testosterone levels in adult male rats 30 days after castration. Furthermore, adrenal androgen production in castrated animals is differentially regulated by sex steroids.