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  • Title: Analysis of estradiol-independent and -dependent endogenous opioid peptide suppression of pulsatile LH release between the mornings of diestrus 2 and proestrus in the rat estrous cycle.
    Author: Babu GN, Bona-Gallo A, Gallo RV.
    Journal: Brain Res Bull; 1988 Aug; 21(2):277-84. PubMed ID: 3191412.
    Abstract:
    The aim of this study was to analyze possible estradiol (E2)-independent and -dependent endogenous opioid peptide (EOP) suppression of pulsatile LH release between the mornings of diestrus 2 (D2) and proestrus by examining the LH response to naloxone infusions in the presence or absence of proestrous levels of E2. Pulsatile LH secretion remained unchanged between D2 and proestrus but mean blood LH levels, pulse amplitude and frequency increased within 24 hr following ovariectomy on D2. This increase was due in large part to the loss of E2 negative feedback, since restoration of physiological proestrous E2 levels returned LH pulse frequency to proestrous a.m. levels and greatly reduced pulse amplitude. In ovariectomized rats lacking E2 negative feedback, continuous infusion of the EOP receptor antagonist naloxone (0.5 and 2 mg/kg/hr) caused a further increase in pulse amplitude and frequency. This naloxone-induced increment in pulsatile LH release was exerted via centrally located EOP receptors since naloxone did not alter pituitary responsiveness to LHRH, and its stimulatory action on pulsatile release was diminished by simultaneous infusion with morphine. Naloxone also increased pulsatile LH release in E2-treated animals. The naloxone-induced increments in LH pulse amplitude were the same in the presence or absence of E2 negative feedback. Moreover, the increments in amplitude produced by naloxone in E2-treated rats were significantly less than those resulting from the combination of ovariectomy plus naloxone infusion in empty capsule-implanted rats. These data indicated that naloxone infusion in E2-implanted animals blocked an E2-independent EOP suppression of this parameter of pulsatile release.(ABSTRACT TRUNCATED AT 250 WORDS)
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