Abstract

Normal male rats, or female rats exposed neonatally to androgens or estrogens, do not respond in adulthood to ovarian hormone treatments that stimulate preovulatory-like surges of luteinizing hormone (LH) or mating behavior in normal females. As an attempt to understand the neurochemical basis for this insensitivity, the present studies tested whether sex differences also exist with respect to several important neural events that are antecedent to and essential for the appearance of an LH surge induced by ovarian hormone treatment. Administration of estradiol via Silastic capsules to adult, gonadectomized rats resulted in a suppression of LH release that was equivalent in males and females, but only the estrogen-primed females responded to injections of progesterone with an LH surge. Similarly, in estrogen-primed females but not males, progesterone induced a presurge sequential accumulation and decline of LH-releasing hormone (LH-RH) concentrations in the median eminence and increased the turnover rates of norepinephrine (NE) and epinephrine (E) in the medial basal hypothalamus during the time of LH-RH accumulation. Ovarian hormones may activate NE and E release in females by removing a tonic inhibition over catecholamine release exerted by endogenous opioids. In order to test whether direct antagonism of opiate mechanisms would produce equivalent neuroendocrine or neurochemical responses in males and females, additional studies tested the effects of the opiate receptor blocker naloxone on LH release and on activity of catecholamines in the medial basal hypothalamus. In contrast to females, estrogen-primed male rats did not display either an increase in serum LH or an enhancement of the α-methyltyrosine-induced decline of NE or E after treatment with naloxone. These data suggest that central noradrenergic and adrenergic systems that control the neurosecretion of LH-RH are insensitive to ovarian hormones in adult male rats, and further, that this may be due in part to fundamental sex differences in the control of catecholamine neurotransmission by hypothalamic opioid systems.

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