Changes in the characteristics of pulsatile LH secretion after estradiol implantation into the preoptic area and the basal hypothalamus in ovariectomized rats.

Abstract

Intracranial actions of estradiol benzoate (EB) in modulating the characteristics of pulsatile LH secretion were examined in ovariectomized rats. A minute amount of crystalline EB was implanted into the medial basal hypothalamus (MBH) or the preoptic suprachiasmatic area (POSC) and blood samples were collected at 6-min intervals for radioimmunoassay of serum LH concentrations. In rats with EB implanted in the MBH, the LH pulse amplitude decreased while the frequency did not change for 3 h after implantation. In rats bearing EB implants in the POSC, in contrast, the LH pulse frequency decreased without a significant variation in the pulse amplitude. Control animals with empty cannulae inserted into the MBH or POSC exhibited unchanged amplitude and frequency of LH secretory pulses. These results indicate that estrogen can regulate the amplitude and frequency of pulsatile LH secretion via mechanisms independent of each other. It appears that MBH and/or the pituitary is a site of the action of estrogen in decreasing LH pulse amplitude, while the POSC is a site of the steroid action in decreasing the pulse frequency.

Influence of Estradiol and Progesterone on Pulsatile LH Secretion in 8-Day Ovariectomized Rats

“…This suggests that the same central mechanisms do not mediate the negative feedback effects of E2 on both parameters of pulsatile LH release. Moreover, implants of E2 into the medial basal hy pothalamus, but not the MPOA, selectively reduced LH pulse amplitude [2], suggesting that E: may work at differ ent central sites to influence the amplitude and frequency of pulsatile LH release.…”

“…There is a lack of agreement in studies in long-term ovariectomized rats as to whether E2 alters only LH pulse amplitude [20, 21.42], pulse frequency [30], or both parame ters of pulsatile LH secretion [2,44], The present data de monstrate that restoration of DI-D2 or D2-proestrous lev els of E2 1 week after OVX suppressed only LH pulse am plitude, whereas our previous results clearly demonstrated that immediate replacement following OVX with D2-proestrous levels of E2 suppressed both LH pulse amplitude and frequency [28], and immediate replacement with D1-D2 levels of E2 had no influence on pulsatile LH secretion [27], Therefore, D2-proestrous levels of E2 retain their sup pressive action on LH pulse amplitude, and D1-D2 levels of E2 remain ineffective in altering pulse frequency. In con trast, D2-proestrous E2 levels lose their suppressive action on LH pulse frequency, and D1-D2 levels of E2 gain the ability to suppress LH pulse amplitude.…”

“…Whereas single injections of estradiol benzoate (EB) will stimulate LH surges in rats ovariectomized for 2 weeks [25], supplemental injections of EB or P are necessary to do so in rats ovariectomized for 4 weeks or longer [8,9,14], and the ability of E2-capsu!es to induce an LH surge decreases with time following OVX [34], Similarly, Dockeet al [15] reported a diminished nega tive feedback of EB on LH secretion when implanted into the medial preoptic area (MPOA) of long-term versus short-term ovariectomized rats, and suggested that this could be due to the longer interval between gonadectomy and treatment. This is of interest since the MPOA has been suggested, albeit in studies employing pharmacological lev els of E2 implanted into this region, to be involved in medi ating the suppressive influence of E2 on LH pulse fre quency but not pulse amplitude [2,3], and the effect of D2-proestrous levels of E2 on pulse frequency but not pulse amplitude is lost by I week after OVX. This suggests the hypothesis that alterations in the actions of E2 in the MPOA following OVX may be involved in the diminished negative feedback of D2-proestrous levels of E2 on LH pulse fre quency.…”

Responses of arcuate neurons to some putative neurotransmitters in perfused rat hypothalamic slices : Effects of in vivo and in vitro estrogen treatments.

“…Estrogen administered in the ovariectomized rat initially suppresses luteinizing hormone (LH) secretion, whereas it later induces LH secretory surge EFFECTS ON ARCUATE NEURONS 693 (LEGAN et al, 1975). It is suggested that the initial negative feedback effect is mainly mediated by estrogen responsive neurons in the MBH (AKEMA et a!., 1983(AKEMA et a!., , 1984 as well as by the pituitary gland (BoGDANOVE, 1963). The delayed action, called positive feedback effect, is mediated by neurons in the preoptic region, but not by those in the MBH (KAWAKAMI et al, 1975;KAWAKAMI and KIMURA, 1976).…”

“…The present study was performed to elucidate how the antidromically identified TI neurons in the arcuate nucleus (ARC), where numerous neuropeptide-and dopamine-containing perikarya have been shown to be present (PALKOVITS, 1982), respond to GABA, glycine, 5-HT, NE, and DA in in vitro preparation of rat hypothalamic slices. The effects of estrogen treatments on the responsiveness of ARC neurons to these agents were also examined, since it has been shown that electrical activity of ARC neurons is affected by estrogen (MAGI, 1973) and that estronge implantation in the ARC causes a change in hormone secretion from the anterior pituitary (AKEMA et al, 1983). A preliminary report of a portion of this study has already been presented (NISHIHARA et al, 1983).…”