The telencephalon and hypothalamus of the bluegill (Lepomis macrochirus): evoked feeding, aggressive and reproductive behavior with representative frontal sections.
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Drosophila melanogaster sex mosaics were tested in their courtship interactions with females and then with males. The distribution of genetically male and female tissues in each mosaic was determined with respect to an external cuticle marker and an internal enzyme marker. Performance of malelike courtship was correlated with the genotype of various tissues, with special attention being paid to the genotypes of head and thoracic ganglia. Male tissue in the left or right dorsal brain is necessary and nearly always sufficient to trigger early courtship actions--following of females and wing extension at them--but male tissue in both the dorsal brain and thoracic ganglia is necessary for attempted copulation to occur. Female tissue on or in the abdomen is nearly always necessary and sufficient for a mosaic to be courted by a male.
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An in vitro radioenzymatic assay and purification procedure by thin-layer chromatography were used to study the metabolism of dihydrotestosterone (DHT) into 3 alpha- and 3 beta-androstanediols by the brain and cloacal gland of Japanese quail. Kinetic studies showed that these 2 metabolites are produced in a linear fashion with respect to time of incubation for up to 15 min but that they continue to accumulate for up to 4 h. The maximum velocity of these reactions is high (nmol/mg protein/15 min), but the affinities of the enzymes for DHT are low (in the microM range). The enzymatic activities are not evenly distributed in the brain: they are high in the tuberal hypothalamus and lobus parolfactorius but low in the preoptic area and anterior hypothalamus. Enzyme activities are not markedly affected by treatment of the birds with either testosterone or DHT. The activity of these enzymes is lower in the preoptic area and tuberal hypothalamus of DHT-treated birds which display female-directed sexual behavior than in the same brain areas of birds which are sexually inactive. We discuss the relationships between this reductive metabolism of DHT and the activational effects of the steroid on sexual behavior.
Neuroactive agents associated with different neurotransmitter systems can modulate the number of hypothalamic estrogen binding sites. It has been demonstrated previously that the muscarinic cholinergic agonist, bethanechol, administered 30 min prior to in vitro estrogen receptor assays increases the concentration of hypothalamic estrogen binding sites by 30-35% in female rats. Bethanechol was without effect on male hypothalamic preparations. In order to investigate further this sex difference and in an attempt to determine a relationship between the modulation of estrogen binding sites and a sexually differentiated function, bethanechol was given to female rats rendered either anovulatory and capable of displaying lordosis or anovulatory and behaviorally insensitive to estrogen. The results showed that bethanechol significantly increased the number of estrogen binding sites in females capable of displaying lordosis but not in females which did not show this estrogen-dependent behavior. It is possible that the capacity for drug-induced modulation of estrogen binding sites could be related functionally to the ability to display lordosis behavior.
The present experiment was undertaken to evaluate the hypothesis that the effects of estrogens on feeding and sexual behaviors are organized separately within the brain. Thirty-three ovariectomized rats were implanted with bilateral guide cannulae aimed at either the paraventricular nucleus (PVN), medial preoptic area (MPOA), or posterior hypothalamus (PH). Subjects that received PVN implants were stimulated with either undiluted estradiol, a 3:1, or 10:1 mixture of cholesterol and estradiol. Animals in the other groups were treated with undiluted estradiol. All females were stimulated unilaterally with cholesterol and estradiol, yielding a total of 66 stimulation sites. Histological analysis revealed that, compared to cholesterol implants, undiluted estradiol in the PVN reduced food intake and body weight. More importantly, diluted estradiol implants in the PVN significantly lowered food intake and body weight. In contrast, undiluted estradiol in the MPOA, PH, or ventromedial hypothalamus (VMH) had no significant effects on feeding or body weight. Analyses of variance revealed significant main effects of implant location on female sexual behavior. Newman-Keuls tests indicated that diluted estradiol implants in the PVN produced lordosis quotients and quality scores that were significantly lower than those obtained with VMH implants. The possibility that the behavioral changes observed were due to peripheral rather than central effects of the hormone was evaluated by comparing the results of implants that produced vaginal cell cornification to those that did not. There were no significant differences between these groups on any of the other dependent variables, indicating that peripheral estradiol sufficient to induce vaginal cell cornification was neither necessary nor sufficient to account for the behavioral changes.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study extends previous studies of ours by comparing the anti-androgenic effect of a progestin agonist (R5020) with progesterone (P). Intact male guinea pigs treated with P (1 and 10 mg/day) and R5020 (100 micrograms/day) had greater latency to mount and lower numbers of mounts and intromissions compared to controls. Ejaculation and plasma testosterone concentration were not affected. Specific brain regions were analyzed for androgen receptor (AR) content. Progestins produced fewer (P less than 0.01) nuclear AR in hypothalamus-preoptic area and pituitary without associated changes in cytosolic AR. These data are best interpreted by postulating an effect of P on AR dynamics mediated through the P receptor and not by competition for androgen binding to its receptor.
A projection from the medial amygdaloid nucleus to the hippocampus and septum probably uses vasopressin as a transmitter. The nucleus synthesizes vasopressin and activation of the nucleus has a hippocampal effect that is completely blocked by a vasopressin antagonist. The afferent and efferent projections of this peptidergic nucleus suggest a possible role for the system in sexual behavior. Stimulation of the nucleus inhibits the output of the hippocampus in both genders and reorganizes behavior for a period of 15-20 min. In males, the effect of peptidergic activation is to produce a behavior that resembles the post-ejaculatory interval in coitus. This state is characterized by an EEG that resembles slow-wave sleep and by ultrasonic vocalizations at a characteristic frequency of 22 kHz. Castration in either gender causes depletion of the peptide from the target fields and eliminates the peptidergic signal in the hippocampus after about 15 weeks. The effects of castration in males can be reversed by testosterone replacement. The fluctuation of estrogen levels in rat plasma during the estrus cycle happens too quickly to impact the peptidergic system, and thus there is no significant change in the strength of the peptidergic signal among the proestrus, estrus, metestrus and diestrus stages. This fact permits study of the physiology of the system without concern for stage of estrus but does not permit conclusions regarding its function in females.
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