Abstract
There is considerable evidence that opioids inhibit luteinizing hormone (LH) secretion via influences upon the noradrenergic system (1,2). The noradrenergic input to the hypothalamus plays an important role in triggering the preovulatory LH surge (3) and drugs that block noradrenaline receptors, or deplete the hypothalamic content of noradrenaline, prevent naloxone-induced LH release (4). By contrast, intraventricular administration of noradrenaline can override morphine-induced suppression of LH (5). This indirect evidence for opioid control of noradrenergic transmission in the hypothalamus has been confirmed by recent in vitro experiments that have demonstrated that noradrenaline release in the preoptic area is inhibited by opioids (6). Luteinizing hormone secretion and the preovulatory LH surge are controlled by neurons in the preoptic and anterior hypothalamic area (PO/AH), and noradrenergic terminals have been found in the proximity of the luteinizing hormone-releasing hormone (LHRH) cell bodies (7,8). The major source of noradrenaline in the hypothalamus is provided by the ventral noradrenergic tract (VNAT) (9). Electrical stimulation of the VNAT increases hypothalamic noradrenaline turnover and evokes LH release (10). Thus this pathway from the brainstem is a likely target for the endogenous opioid influence on LH secretion.KeywordsLuteinizing HormonePreoptic AreaLuteinizing Hormone SecretionNaloxone AdministrationOpioid Antagonist NaloxoneThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Published Version
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