Steroid-independent endogenous opioid peptide suppression of pulsatile luteinizing hormone release between estrus and diestrus 1 in the rat estrous cycle

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We have previously demonstrated an absence of ovarian steroid negative feedback on pulsatile luteinizing hormone (LH) release between estrus and early diestrus 1 (D1) in the rat estrous cycle. The object of the present study was to determine if there was a steroid-independent endogenous opioid peptide (EOP) suppression of pulsatile LH release in thes same 24-h interval, and if so, which parameter(s) of pulsatile LH release were affected. Rats were bled on estrus, or 24 h following sham ovariectomy (OVX), or OVX at 08.30–10.00 h on estrus. At the time of bleeding all rats were infused i.v. for 4 h either with 0.9% saline (0.5 ml/h) or naloxone (0.005, 0.05, 0.5, or 2 mg/kg/h). At 1 h after the infusion began, rats were bled for 3 h (40 or 50 μl whole blood/5 min) between 09.30 and 12.30 h. Mean blood LH levels increased between estrus and early D1 due to increases in LH pulse amplitude and frequency. OVX on estrus decreased plasma levels of estradiol and progesterone 24 h later, but did not augment the increase in pulsatile LH release. However, naloxone infusion augmented the increase in pulsatile LH secretion in sham ovariectomized rats in a dose-dependent fashion. While infusion of 0.005 or 0.05 mg/kg/h had no effect, 0.5 or 2 mg/kg/h increased blood LH levels by increasing both LH pulse amplitude and frequency. The stimulatory effect of naloxone on pulsatile LH release was blocked by simultaneous infusion of morphine, demonstrating that the effect was mediated by EOP receptors. In addition, pituitary responsiveness to LHRH in vivo was not altered by naloxone infusion, indicating a central site of action for the EOP receptor antagonist. These data confirm our previous report that the increases in LH pulse amplitude and frequency occuring from estrus to early D1 occur in the absence of ovarian steroid negative feedback. However, pulsatile LH release would increase even further in this time interval were it not for the existence of a centrally occurring, steroid-independent EOP suppression of both LH pulse amplitude and frequency during this 24-h period of the rat estrous cycle.