Norepinephrine (NE) and dopamine (DA) activities were measured in several discrete brain areas (medial preoptic nucleus, suprachiasmatic nucleus, median eminence, and arcuate nucleus) in ovariectomized (OVX) and OVX steroidtreated rats. We wished to determine whether catecholamine (CA) mechanisms are involved in estradiol (E2)-induced LH surges and if amplification of such surges by progesterone (P)affects these CA systems. Animals were OVX, and 1 week later (day 0), groups were treated with Silastic capsules containing oilor an E2 solution (150 μg/ml in sesame oil). At 0900 h on day 2, E2-treated animals received Silastic capsules containing oil or P (50 mg/ml in oil). This steroid treatment results in physiologicalserum concentrations of both steroids. CA concentrations were determined by radioenzymatic assay in animals killed at 1000 or 1500 h on day 2 and in animals which were sacrificed 2 h after receiving a-methyl paratyrosine (400 mg/kg) at 1000 or 1500 h. Serum LH, FSH, PRL, E2, and P concentrations were measured by RIA. E2-induced LH surges were accompanied by increased NE turnover rates in all brain areas examined during the afternoon of day 2. P temporally advanced and enhanced the LH surge during the afternoon of the day that it was administered, and this effect was correlated with an advancement of increased NE turnover rates in the suprachiasmatic nucleus and median eminence. DA turnover rates were elevated in the median eminence and arcuate nucleus of steroid-treated animals compared to those in OVX rats, but there was no change during the afternoon when gonadotropin and PRL surges were occurring. Seemingly, E2-induced gonadotropin and PRL surges are mediated by increased NE activity. Further, increased NE activity in the suprachiasmatic nucleus and median eminence is advanced in time in E2- and P-treated rats, which suggests that the effect of P on the timing and amplitude of the LH surge may also involve a noradrenergic mechanism. In contrast, decreases in tuberoinfundibular DA activity do not seem to be critical for steroid-induced gonadotropin surges to occur.
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