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      Long-Term Weekly Gonadal Steroid Treatment: Effects on Plasma Prolactin, Sexual Behavior and Hypothalamic-Preoptic Area Catecholamines

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          Treatment of intact female rats with weekly injections of estradiol benzoate followed 48 h later by progesterone reliably induced high levels of sexual behavior. After 15–20 treatments, 25% of one group of females became refractory to the sexual-activity-inducing effects of ovarian steroids. The apparent deficit in sexual behavior could not be attributed to variation in prolactin secretion, as long-term steroid treatment resulted in greatly elevated circulating prolactin levels (>1 µg/ml) which were equivalent in good sexual responders (lordosis quotient, LQ ≧ 90) and sexually refractory females (LQ ≤ 20). In control rats, short-term steroid treatment (5 weeks) decreased dopamine (DA) and dihydroxyphenylacetic acid (Dopac) concentrations in the median eminence (ME) and induced good sexual behavior. Interestingly, a similar pattern of decreases in DA and Dopac levels of ME was observed in those long-term-treated rats displaying good sexual behavior but not in the sexually refractory females. Further, a significant increase in DA concentration in the preoptic-an-terior hypothalamic area of the sexually refractory females was observed. These data are interpreted to suggest that (1) severe and chronic elevations in circulating levels of prolactin, induced by chronic ovarian steroid treatment, are not universally associated with a disruption of sexual behavior and (2) increased dopaminergic function in the ME, seen in females with normal sexual behavior, was conspicuously absent in female rats that became refractory to the sexual-behavior-inducing effects of ovarian steroids.

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          Author and article information

          S. Karger AG
          01 April 2008
          : 44
          : 4
          : 488-493
          aDepartment of Obstetrics and Gynecology, University of Florida College of Medicine; and bDepartment of Pharmacodynamics, University of Florida College of Pharmacy, Gainesville, Fla., USA
          124691 Neuroendocrinology 1986;44:488–493
          © 1986 S. Karger AG, Basel

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          Pages: 6
          Original Paper


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