Alpha-methyltryptamine, a drug which stimulates serotonergic receptors in the central nervous system, inhibited the induction of sexual receptivity in spayed female rats by estradiol benzoate and progesterone. The drug had no effect on the sexual receptivity induced by estradiol benzoate alone. These data are consistent with the hypothesis that progesterone facilitates lordosis in estrogen-primed rats by inhibiting a serotonergic system in the brain. The data also suggest that estradiol and progesterone act on separate neurochemical systems to induce estrous behavior in rats.

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PubMedDate not supplied

Effects of cold exposure on estrous behavior and neural estrogen receptor in Syrian hamsters.

Two experiments examined the effects of 72-h exposure to reduced environmental temperature (5 degrees C) on steroid-induced estrous behavior and neural estrogen-receptor immunoreactivity (ERIR) in ovariectomized Syrian hamsters. Cold exposure significantly inhibited sexual receptivity induced by sequential injections of estradiol benzoate (2.5 microg) and progesterone (500 microg), but only if the animals were not permitted to overeat (limited to 110% of ad lib intake at 22 degrees C). The suppression of sexual receptivity was accompanied by decreases in the number of detectable ERIR cells in the ventromedial hypothalamus (VMH) and by increases in the number of ERIR cells in the medial preoptic area (mPOA). The cold-induced decreases in estrous behavior and in VMH ERIR cells were prevented by lesions of the area postrema (AP), but AP lesions did not prevent the increases in mPOA ERIR cells. Thus, cold exposure mimics the effects of treatment with metabolic inhibitors, experimental diabetes, food deprivation, and insulin-induced fattening on these endpoints. These findings are consistent with the hypothesis that dwelling in the cold affects reproduction indirectly via its actions on metabolic fuel availability, rather than by acting directly on neuroendocrine processes.

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