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The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.

Two ovarian hormones, estradiol and progesterone, which facilitate mating behavior in the female rat by acting on the ventromedial nuclei (VMN) of the hypothalamus, induce changes in oxytocin receptor binding in this brain region. Estradiol induced a 4-fold increase in the oxytocin receptor binding of the VMN and surrounding area and increased the number and immuining ofoxytocin fibers in an area lateral to the ventral VMN. Progesterone, in estrogen-primed rats, caused the induced oxytocin receptors to spread over the area containing the oxytocin fibers. Infusion of oxytocin into the ventromedial hypothalamus increased the display of lordosis behavior only in females primed with both estradiol benzoate and progesterone. Thus, the sequential actions of two ovarian hormones bring a neuropeptide and its receptors into register and enable the neuropeptide to exert behavioral effects.Oxytocin (OT) is a hypothalamic neuropeptide implicated in systemic and neural events related to pregnancy, parturition, and maternal behavior (1, 2). Recent evidence suggests that OT also facilitates feminine mating behavior in rodents (3-5).Estradiol (E) and progesterone (P) sequentially activate mating behavior (lordosis) in the female rat by acting at the level of the ventromedial nuclei (VMN) ofthe hypothalamus (6, 7). E treatment induces two prominent neurochemical changes in the VMN that may be related to the activation of lordosis behavior-namely, induction of progestin receptors (8, 9) and oxytocin receptors (10). P actions on mating behavior require prior estrogen priming (11). However, the cellular and molecular mechanisms by which P potentiates the behavioral effects ofestrogens are poorly understood. Their understanding would help to explain the synergy of E and P action on the brain. In this study, we examined the influence of P in E-primed rats on the density and area of OT receptors in VMN, on immunostaining for OT in the ventral hypothalamus, and on lordosis behavior elicited by OT infusion into the VMN region. MATERIALS AND METHODSAnimals and Treatments. Female Sprague-Dawley rats (250 g) were used. Rats were housed three animals per cage in an inverse light/dark cycle (lights on at 6 p.m.; lights off at 8 a.m.) throughout all experiments. Food and water were available ad libitum.Experiment 1 (OT Receptor Binding). Rats were ovariectomized and adrenalectomized 4 days before starting the hormone treatment on day 1 under methoxyflurane (Metofane) anesthesia, and the drinking water was replaced by 0.9%o saline. Females were distributed randomly between the following experimental groups: control females (C group, n = 6), females treated with estradiol benzoate (EB; Sigma) (EB group, n = 6), females treated with both EB and P (Steraloids) (EB+P group, n = 6), and females treated with P (P group, n = 5). EB-and EB+P-treated females were injected subcutaneously (s.c.) twice with 10 ug of EB dissolved in 100 ILI of sesame oil in the morning of day 5 and day 6, respectively. The two other groups were injected with vehic...

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Oxytocin (OT) neurotransmission plays a role in the facilitation of steroid-dependent sexual receptivity in the rat. One way in which the ovarian steroid 17 beta-estradiol (E2) has been shown to modulate OT transmission is by increasing OT receptor binding in certain brain areas involved in the regulation of female sexual behavior such as the ventromedial hypothalamic nucleus (VMN). This study was undertaken to describe the distribution of OT receptors within the VMN that are regulated by physiological levels of E2. With quantitative autoradiographic methods, we measured [3H]OT binding in ovariectomized female rats implanted with Silastic capsules containing cholesterol, 5% E2, or 100% E2. In addition, plasma E2 levels, pituitary progestin receptor binding, and uterine weights were measured in animals from each treatment group. Results of this study showed that physiological levels of E2 increased [3H]OT binding in caudal regions of the ventrolateral VMN and stimulated maximal uterine growth and pituitary progestin receptor binding. However, in more rostral VMN sections, E2 induced a dose-dependent increase in [3H]OT binding. These data suggest that ovarian steroids sensitize the brain to OT by increasing OT receptor binding in certain brain areas involved in the regulation of sexual receptivity.

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Oxytocin (OT) transmission is involved in the steroid-dependent display of sexual receptivity in rats. One of the biochemical processes stimulated by the ovarian steroid 17 beta-estradiol (E2) that is relevant to reproduction is the induction of OT receptor binding in the ventromedial hypothalamic nucleus (VMN). The purpose of these experiments was to determine if E2-induced changes in OT receptor binding in the VMN occur within a time frame relevant to cyclic changes in ovarian steroid secretion. OT receptor binding was measured in the VMN of ovariectomized rats implanted for 0-96 h with E2-containing Silastic capsules. The rate of decay of OT receptor binding was measured in another group of animals 6-48 h after capsule removal. Receptors were labeled with the specific OT receptor antagonist [125I]d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT, and binding was measured with quantitative autoradiographic methods. In addition, plasma E2 levels and uterine weights were assessed in animals from each treatment condition. Significant increases in E2-dependent OT receptor binding and uterine weight occurred within 24 h of steroid treatment. After E2 withdrawal, OT receptor binding and uterine weight decreased significantly within 24 h. These results are consistent with the hypothesis that steroid modulation of OT receptor binding is necessary for the induction of sexual receptivity.