[Studies on the feedback regulation of pulsatile luteinizing hormone secretion. II. Role of the catecholaminergic system in estrogen-induced suppression of the frequency of pulsatile LH secretion in ovariectomized rats].

The pattern of pulsatile secretion of luteinizing hormone (LH) is affected by the circulating gonadal hormone levels. In the rat the frequency and amplitude of the LH pulse increase after ovariectomy and decrease after estrogen replacement. Since estrogen is known to affect the catecholaminergic activities in the rat hypothalamus, the present study examined whether the catecholaminergic mechanisms are involved in the estrogen-induced suppression of pulsatile LH secretion. Recently, we have elucidated that the preoptic suprachiasmatic area (POSC) is a specific site of action of estradiol in reducing the LH pulse frequency. Subsequently, in this paper, we report the effects of various catecholamine synthesis inhibitors and synaptic blockers on the basal pulsatile LH secretion and on the frequency suppression induced by local implantation of EB in the POSC. Female rats of the Wistar strain were ovariectomized about 4 weeks before the experiment. Blood samples were obtained at 6-min intervals for 4 h without anesthesia through the indwelling atrial catheter. The rats were given i.p. injection with the drug or the vehicle 1 or 3h before bleeding. The steroid was implanted into the POSC via the chronically-implanted cannula 1 h after the initiation of the bleeding. Serum LH concentrations were determined by radioimmunoassay. The following results were obtained. EB implantation into the POSC suppressed the frequency of existing pulsatile LH secretion in vehicle-treated rats. Pretreatment of the rat with alpha-methyl-p-tyrosine (AMPT), AMPT + threo-dihydroxyphenylserine (DOPS) or pimozide did not affect the basal pulsatile LH secretion but prevented suppressive effect of EB implantation on the LH pulse frequency. In rats pretreated with diethyldithiocarbamate (DDC) or phenoxybenzamine the basal pulsatile LH secretion was abolished. Further suppression by EB implantation was not clear. Pretreatment of the rats with propranolol did not affect the basal pulsatile LH secretion nor the EB-induced suppression of the LH pulse frequency. These results support the hypothesis that the alpha-adrenergic mechanism is required for maintaining the basal pulsatile LH secretion in ovariectomized rats. Furthermore, the dopaminergic system is obligatorily necessary for the manifestation of the inhibitory action of EB implanted in the POSC on the LH pulse frequency.