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      Modulation of Luteinizing Hormone Release and Catecholamine Activity by Opiates in the Female Rat

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          Previous studies have shown that the stimulation of LH release by the opiate receptor blocker, naloxone, can be prevented by catecholamine synthesis inhibitors, suggesting opiate regulation of catecholamine release. The present study tested whether an opiate agonist and antagonist would affect the depletion of hypothalamic catecholamines observed after synthesis inhibition, as a measure of catecholamine activity, concomitant with changes in LH secretion. Administration of naloxone to estradiol-primed rats increased LH release and potentiated the depletion of norepinephrine in the preoptic-anterior hypothalamus and medial basal hypothalamus, and enhanced the decline of epinephrine and of dopamine in the medial basal hypothalamus, suggesting increased catecholamine activity in these regions. Administration of the opiate agonist, morphine, to estrogen/progesterone pretreated females decreased LH and decreased the depletion of the catecholamines in the above mentioned areas, suggesting reduced activity. In most cases, naloxone antagonized the inhibitory effect of morphine. These findings indicate that naloxone may stimulate LH release by enhancing hypothalamic catecholamine turnover, possibly by removing the inhibitory influence of an endogenous opioid neuropeptide.

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          S. Karger AG
          28 March 2008
          : 38
          : 3
          : 248-253
          Department of Pharmacology, University of Tennessee, Center for the Health Sciences, Memphis, Tenn., USA
          123899 Neuroendocrinology 1984;38:248–253
          © 1984 S. Karger AG, Basel

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          Pages: 6
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