A surge of gonadotropin-releasing hormone accompanies the estradiol-induced gonadotropin surge in the rhesus monkey.

In several species, the ovulatory LH surge is preceded by a surge of GnRH. Although a role for estradiol in the initiation of the LH surge is well established in the primate, several observations in the rhesus monkey have questioned whether such an estradiol-induced neurosecretory event takes place. We report on GnRH measurements in cerebrospinal fluid (CSF) samples obtained from the third ventricle of intact and ovariectomized (OVX) conscious rhesus monkeys during control periods and throughout the estradiol-induced positive feedback phase. In the first experiment, we measured control GnRH concentrations in CSF collected at 15-min intervals uninterruptedly for a period of 1-5 days in tethered OVX monkeys (n = 4) in their cages without steroid priming. As had been demonstrated previously with the same method in restrained animals, CSF from the third ventricle contained detectable amounts of GnRH. Spontaneous GnRH secretion was pulsatile; overall mean pulse interval was 67.4 (+/- 2.2 SE) min for a total of 177 GnRH pulses. During 2 periods (8 and 6 h) when simultaneous blood and CSF samples were obtained, 14 out of 15 GnRH pulses were accompanied by an LH pulse. To evaluate the effects of an estrogen challenge on GnRH secretion, estradiol benzoate (E2B; 330 micrograms) was given to 4 intact (5 experiments) and to 2 OVX monkeys. CSF collection was initiated 8-24 h before E2B injection and continued for 72-84 h thereafter. E2B administration resulted in a surge of LH and of GnRH in all but one experiment. The mean time of onset of the GnRH surge was 22.0 (+/- 4.0) h after E2B, whereas that of the LH surge was 24.7 (+/- 3.4) h. In contrast to LH, which declined after a peak at 35.2 +/- 3.9 h, the increase in GnRH secretion persisted throughout most of the observation period. The magnitude of the GnRH response differed in the 2 groups; in the intact animals, mean peak GnRH concentration increased 8.9-fold but only 3.8-fold in the OVX monkeys. A similar GnRH surge was observed in 1 OVX monkey, receiving an iv infusion of E2, which produced more physiological concentrations of E2. In this animal, an initial suppression of GnRH concentration in the 24-48 h period after E2 (GnRH control, 14.6 +/- 1.9; post-E2, 4.0 +/- 0.5 pg/ml) preceded the initiation of the GnRH surge which occurred at 54 h after E2.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects and site of action of morphine on gonadotropin secretion in the female rhesus monkey.

The effects of morphine on gonadotropin secretion, and the site of its action, were tested in female rhesus monkeys. In Exp 1, morphine sulfate (3, 6, or 9 mg iv) was injected into ovariectomized monkeys, and its effects on tonic (pulsatile) LH and FSH secretion were examined. Administration of morphine (9 mg) resulted in a significant decrease in circulating LH and FSH, which lasted for 4-5 h. Exp 2 was performed to evaluate the site of action of morphine, whether hypophyseal or suprahypophyseal. The effects of morphine (6, 9, or 12 mg) on the LH response to GnRH pulses were evaluated in stalk-sectioned monkeys, in which gonadotropin secretion had been restored by long term pulsatile infusion of GnRH. LH responses to GnRH were not significantly altered by morphine. Exp 3 was performed to determine the effects of morphine on the estrogen-induced LH surge. Estradiol benzoate (330 micrograms in oil) was administered on days 2-5 of the menstrual cycle to nine animals. Four of these also were injected with 9 mg morphine at 5-h intervals for 40 h. Four of the five control and three of the four morphine-treated monkeys showed similar LH surges. The results demonstrate that, in the monkey, opiates inhibit tonic (pulsatile) gonadotropin secretion, most probably by acting at a suprahypophyseal site. In contrast, morphine does not alter the estradiol-induced LH surge, a result that differs from that seen in lower species and that may be related to differences in estradiol positive feedback characteristics.