No abstract

The aim of this study was to determine whether the rapid increases in LH pulse amplitude and frequency that occur within 24 h after ovariectomy (ovx) on diestrus day 1 (D1) were due to the removal of progesterone (P) and/or estradiol (E). Initial studies demonstrated that plasma levels of E and P were 18.2 +/- 1.2 pg/ml and 34.1 +/- 3.2 ng/ml, respectively, between the evening of D1 and the morning of D2 in our colony of intact rats. Immediately after ovx and jugular venous cannulation on the morning of D1, rats were implanted either with empty Silastic capsules or capsules capable of restoring physiological levels of E and P to the control values reported above. These rats were continuously bled (75 microliter/6 min) for 3 h 1 day after ovx for analysis of pulsatile LH release, and then additional plasma samples were gathered for determination of E and P levels. Rats with empty capsules had decreased levels of E and P and increases in mean blood LH levels, LH pulse amplitude, and pulse frequency. Animals with E capsules had physiological levels of E and decreased levels of P, but no suppression of the acute post-ovx increase in pulsatile LH release. In contrast, animals with P capsules had physiological plasma levels of P, decreased levels of E, and a marked reduction in the acute LH response to ovx. This suppression was due entirely to a decrease in LH pulse amplitude, as pulse frequency was not altered. Rats with E and P capsules had physiological levels of these hormones, which resulted in an even greater reduction in the acute LH response to ovx. This suppression was due to decreases in both LH pulse amplitude and pulse frequency. The effect of P on LH pulse amplitude was centrally mediated, since the in vitro response to LHRH of anterior pituitary fragments from P-implanted rats was the same as that of anterior pituitary fragments taken from rats with empty capsules. These studies demonstrate that the acute increase in LH pulse amplitude that occurs within 24 h after ovx on D1 is due to the absence of a central inhibitory effect of ovarian P, while the rapid increase in LH pulse frequency is due to the loss of both ovarian E and P.(ABSTRACT TRUNCATED AT 400 WORDS)

The object of this study was to determine the influence of ovarian steroids on pulsatile LH release in the interval between the mornings of diestrus 2 (D2) and proestrus in the rat. Four groups of rats were bled continuously for 3 h between 09.30–12.30 h at a rate of 75 µl whole blood/6 min: (1) bled on D2; (2) sham ovariectomy (OVX) on D2 and bled on proestrus; (3) OVX on D2, implanted with empty or oil-filled capsules, and bled 24 h later; and (4) OVX on D2, implanted with estradiol (E2) capsules, and bled 24 h later. Between D2 and proestrus, plasma E₂ levels increased from 13 ± 1 to 42 ± 9 pg/ml, and progesterone levels decreased from 27 ± 3 to 13 ± 2 ng/ml, the latter reflecting the decline of the corpus luteum early on D2. Between D2 and proestrus there was no change in mean blood LH levels, LH pulse amplitude, or pulse frequency. However OVX on D2 increased mean blood LH levels 2.5-fold over values on proestrus due to a 3.5-fold elevation in LH pulse amplitude and an 80% increase in pulse frequency. E₂ levels fell in these rats to 8 ± 1 pg/ml. Restoration of physiological proestrous levels of E₂ (46 ± 5 pg/ml) significantly reduced the increase in mean blood LH levels by lowering pulse frequency to proestrous values, and by causing a 50% reduction in pulse amplitude. However, LH pulse amplitude and therefore mean blood LH levels were still higher than values on proestrus. The possibility that ovarian progesterone might also regulate LH pulse amplitude in the D2-proestrous interval was ruled out since there were no significant differences in plasma progesterone levels between 13.00–19.00 h following sham OVX or OVX of rats earlier on the morning of D2. In vitro incubation studies with anterior pituitaries from rats ovariectomized 24 h prior on D2 and implanted with E₂ or empty capsules demonstrated that E₂ increased the pituitary sensitivity to LHRH, indicating that the E₂-induced decrease in LH pulse amplitude could not be exerted at the pituitary level. In conclusion, since LH pulse amplitude and frequency remain unchanged between the mornings of D2 and proestrus, yet increase following OVX, the present data demonstrate that ovarian E₂ acts centrally to exert a restraining effect on both parameters of pulsatile LH secretion during this interval in the rat estrous cycle.

These experiments examined the time course of changes in the characteristics of pulsatile luteinizing hormone (LH) secretion that occur after ovariectomy (OVX) in the rat, and compared the response of the brain and pituitary to the absence of ovarian steroid negative feedback. The literature indicates that the brain could respond to OVX by altering the frequency and/or amplitude of the pulsatile luteinizing hormone releasing hormone (LH-RH) release which triggers pulsatile LH secretion, while the pituitary could respond by altering basal LH output and/or its response to LH-RH. In vivo experiments examined changes in mean blood LH levels, LH pulse amplitudes and pulse frequencies in control rats on diestrus 1 (Dl) and at 7 h, 14 h, 1, 2 or 8 days, or 3 weeks following OVX. In addition, anterior pituitaries from rats on Dl or rats ovariectomized for 1, 2 or 8 days, or 3 weeks, were incubated in vitro with or without LH-RH to examine changes in both basal and LH-RH-induced LH release.

We addressed the question of how rapidly gonadal steroids might affect behavior by studying how fast testosterone (T) could augment the actions of the striated penile muscles and their associated penile reflexes. Eight male rats, functionally castrated 4 months before this study, bore chronically implanted electrodes in the bulbospongiosus (bulbocavernosus) muscle. The males were observed for the display of penile reflexes immediately after the injection of T (250 µg i.m.) and T propionate (250 µg s.c), as well as after injections of only the oil vehicle. Overt penile responses were rare. However, in several tests subcutaneous twitching was observable near the midline posterior to the penis. These twitches were accompanied by electromyographic bursts and were attributed to contractions of the bulbospongiosus muscle. T reliably (p < 0.025) accelerated the onset of electromyographic activity: 6 of the 8 males had electromyographic bursts before the 30-min limit, and 3 males responded within 6 min. This is the first demonstration of such a rapid action of androgens on behavior or its basis in striated muscle activity. The rapid muscular response to T was ascribed to steroid-sensitive neuronal membrane receptors. Such responsiveness could increase the intensity of penile reflexes within minutes after surges of luteinizing hormone and T have been induced by cues associated with estrous females and thereby could contribute to the fertility of mating.