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      Different Neuroendocrine Mechanisms Regulate the Acute Pituitary Follicle-Stimulating Hormone Response to Orchidectomy and Ovariectomy

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          The following experiments were conducted to determine whether a sex difference exists in neuroendocrine mechanisms controlling acute pituitary follicle-stimulating hormone (FSH) responses to castration. Adult male rats and 4-day cycling female rats on diestrus 1 were injected intraperitoneally with either phenobarbital sodium (PhB, 80 mg/kg b.w.) or vehicle at 08.00 h. Following a blood collection at 10.00 h, rats given PhB or vehicle were either sham castrated or castrated under ether. Additional blood samples were obtained, and supplemental PhB or vehicle injections were given at 3, 8, 13, 18, and 24 h after castration. Administration of PhB to male rats completely prevented acute increases in plasma luteinizing hormone (LH) and FSH levels after orchidectomy (ORDX). In contrast, PhB treatment did not prevent initial rises in plasma FSH levels at 8 h after ovariectomy (OVX) and only partially suppressed OVX-induced increases in plasma FSH levels between 13 and 24 h. Plasma LH levels were not elevated by 24 h after OVX. In order to specifically evaluate the role of LH-releasing hormone (LHRH) in mediating the PhB-sensitive rises in gonadotropins after castration, groups of male rats and female rats on estrus were injected subcutaneously with 400 µg of a potent LH-RH antagonist (ALHRH) or oil at 12.00 h. At 10.00 h on the next morning, an initial blood sample was taken, and all rats were castrated under ether. Additional blood samples were taken at times indicated in the previous experiment. Similar to PhB, ALHRH completely abolished ORDX-induced increases in circulating LH and FSH levels. In contrast to PhB, ALHRH partially suppressed increases in plasma FSH levels 8 h after OVX. Similar to PhB, however, ALHRH partially suppressed FSH levels between 13 and 24 h. In a final experiment, FSH release was observed to be episodic 20–24 h after either ORDX or OVX, but not 8–12 h after OVX. Taken together, these results clearly demonstrate that acute increases in nonepisodic FSH secretion after ORDX are totally mediated by LHRH. In contrast, acute increases in the nonepisodic component of FSH secretion after OVX are due to both an LHRH-dependent and LHRH-independent mechanism (i.e., increase in basal FSH secretion). Finally, in view of the LHRH-independent control of pulsatile FSH release, the present results suggest that central mechanisms regulating episodic discharges of FSH become activated between 13 and 24 h after OVX.

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          Author and article information

          S. Karger AG
          01 April 2008
          : 43
          : 4
          : 511-518
          Department of Physiology, University of Texas Health Science Center, San Antonio, Tex., USA
          124575 Neuroendocrinology 1986;43:511–518
          © 1986 S. Karger AG, Basel

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          Pages: 8
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