Forebrain sites of estradiol-17 beta action on sexual behavior and aggression in female Syrian hamsters.

The effects of intracranial implants of estradiol in the ventromedial hypothalamus (VMH), the anterior hypothalamus (AH), or the medial amygdala (AMG) on aggression, sexual behavior, and serum estradiol were examined in female Syrian hamsters. Estradiol implants in the VMH, followed by systemic progesterone, stimulated sexual behavior and inhibited aggression. Estradiol implants in other intracranial sites activated sexual behavior but did not reliably inhibit aggression. Intracranially implanted and systemically treated animals had equivalent peripheral estradiol concentrations at sacrifice. These results suggest that: (a) the VMH is an important neural site for estradiol actions on sexual and aggressive behavior, (b) the caudal AH and AMG also may be sites of estradiol action on sexual behavior, and (c) these intracranial implants may only be effective given systemic estradiol exposure or the concurrent stimulation of multiple brain areas.

A retrograde tracer strategy using True Blue to label the preganglionic parasympathetic innervation of the abdominal viscera.

A simple and reliable method for labeling the preganglionic neurons which innervate the abdominal viscera is described. Infusion of a True Blue (TB) suspension in several different concentrations directly into the peritoneal cavity consistently labeled the medullary vagal nuclei including the dorsal motor nucleus (DMN), nucleus ambiguus (NA), and retrofacial nucleus (RFN). Quantitative analysis of cell labeling after 30 microliters infusions of a large range of concentrations of TB (0.001-20.0%) showed that: (1) as little as 0.0075 mg of TB was sufficient to label DMN cells distinctly while only 0.075 mg (or larger) doses of TB were adequate for labeling cells of the NA and the RFN, and (2) doses of 3.0 mg (or greater) labeled the maximum number of cells in the DMN, NA, and RFN. Qualitative analysis suggested that medium range doses (0.075-0.75 mg) were optimal for discerning cell size and type throughout each of these nuclei.

Progesterone inhibition of sexual behavior is accompanied by an activation of aggression in female Syrian hamsters.

Previous studies have shown that progesterone can have biphasic activational and inhibitory roles in the regulation of sexual behavior in female Syrian hamsters. The purpose of this study was to determine whether these biphasic effects on sexual behavior are mirrored in a reciprocal regulation of aggression. Ovariectomized female Syrian hamsters were treated with estradiol followed 2 and 3 days later by either 1) two oil injections (O-O), 2) an oil and a progesterone injection (O-P), 3) a progesterone and oil injection (P-O), or 4) two progesterone injections (P-P). Females were tested for aggression and sexual behavior in conjunction with these hormone treatments. On the final test session, P-P females had significantly lower lordosis durations than did O-P females, confirming the progesterone inhibition of sexual behavior previously reported. Without hormone treatment all females showed high baseline levels of aggression. On the last behavioral test, aggression in O-O females and P-O females was comparable to their baseline levels of aggression. In contrast, aggression in P-P females was significantly higher than the baseline levels of aggression. These results suggest that like its effects on sexual behavior, progesterone can have both inhibitory and activational effects on aggression in female Syrian hamsters.

Steroid treatment fails to induce an afternoon luteinizing hormone or prolactin surge in rats exposed to short-term constant light at the time of ovariectomy.

The present study investigated the effects of short-term exposure to constant light, initiated at the time of ovariectomy, on the ability of estradiol (E2) treatment alone or in conjunction with progesterone (P) to induce afternoon surges of LH and prolactin (PRL). Adult Fischer 344 rats, which had been ovariectomized (OVX) and placed into constant light (LL) on day 0, were implanted with Silastic capsules containing E2 on day 7 and an atrial cannula on day 8. On the following day (day 9), hourly blood samples were collected between 12.00 and 20.00 h from LL-exposed animals which had received E2 treatment alone or from LL E2-treated animals which had also received P at 12.20 h. Blood samples from control animals which were OVX and treated with E2, but maintained under a 12-hour light:12-hour dark photoperiod, were also collected. Exposure to 9 days of LL abolished the ability of E2 treatment to induce an afternoon surge of LH or PRL. The addition of P treatment to LL E2-treated animals failed to reinstate an LH or PRL surge. While P treatment in LL E2-treated animals induced a rise in PRL levels, it is unlikely, given the timing, duration, and magnitude of PRL release, that this enhancement was initiated by the same mechanisms which normally generate the afternoon surge. The results from the present study demonstrate that short-term exposure to LL, initiated at the time of OVX, abolishes the E2-induced afternoon surges of LH and PRL.

Differential hormonal control of aggression and sexual behavior in female Syrian hamsters.

These experiments were designed to test the effects of chronic estradiol treatment on aggression and sexual behavior in female hamsters. Isolated female hamsters were ovariectomized and tested for their behavioral responses to a group-housed, ovariectomized female hamster (aggression test) and a group-housed, intact male hamster (sexual behavior test). Following these baseline tests, the experimental females were implanted sc with Silastic capsules containing different concentrations of estradiol (100, 25, 10, or 0%) diluted with cholesterol and retested 3, 7, 10, and 14 days after implantation. High levels of aggression were observed on the baseline test, with no changes in aggression toward an intruder female observed for any implant group on subsequent tests. Despite these high levels of aggression toward another female, most of the estradiol-treated females (80% at 14 days) were sexually responsive in the presence of a male. There was no effect of Silastic estradiol concentration on sexual behavior, even though a range of serum estradiol levels (39-105 pg/ml) resulted. Lordosis latencies decreased and lordosis durations increased over the extent of estradiol treatment. Seventeen days after Silastic implantation, all females were injected with progesterone and restested. Estradiol-treated females showed an extreme reduction in aggression toward a stimulus female, as well as a further stimulation of sexual behavior after progesterone treatment. High levels of aggression in cholesterol-treated females (0% estradiol) were maintained even after progesterone injection, and these females never displayed any sexual responsivity. These results suggest that sexual behavior in the female hamster is sensitive to estradiol alone, whereas the inhibition of aggression requires the combination of estradiol plus progesterone.