Unlike other rodents, juvenile female guinea pigs rarely display sexual receptivity (lordosis) following a variety of estradiol and progesterone treatments that elicit estrous behavior in adult females. The long-range goals of the experiments described in this application are to elucidate the neural mechanisms underlying the behavioral hyporesponsiveness to steroid hormones in immature females. The primary foci of this proposal are a caudally-projecting, steroid responsive pathway originating in the hypothalamus that appears to mediate the behavioral actions of estradiol and progesterone, the neurotransmitters acting within this pathway, and the activity of other central nervous system components, particularly one originating in or traversing the medial preoptic area, that may inhibit or override its activity, during the juvenile period. A combination of physiological, pharmacological and neuroanatomical techniques will be used to determine the integrity, in juvenile females, of the putative pathways mediating steroid-induced lordosis. Several neurotransmitter systems will be studied, to ascertain whether hypoactivity in neurotransmitter systems thought to be stimulatory for lordosis (norepinephrine, substance P) or hyperactivity of systems thought to inhibit receptivity (endogenous opiates) might underlie the juvenile female's immature behavioral response to steroid hormones. The results of these studies will provide insight into the mechanisms of steroid hormone action in the central nervous system, especially within the context of puberty. These data will help establish a framework within which one can study normal, as well as aberrant sexual maturation and/or responsiveness to estradiol and progesterone in humans and laboratory animals.
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