Effects of estradiol benzoate on catecholamine levels and turnover in discrete areas of the median eminence and the limbic forebrain, and on serum luteinizing hormone, follicle stimulating hormone and prolactin concentrations in the ovariectomized female rat

The effects of estradiol benzoate (E₂B) on brain catecholamines (CA) and serum gonadotropins and prolactin were studied in the ovariectomized rat. The levels of noradrenaline (NA) and dopamine (DA) in the median eminence (ME) and the forebrain (F) were studied using micro-fluorimetry. CA turnover was determined by rates of CA disappearance after tyrosine hydroxylase inhibition. The following areas were studied in the ME: the subependymal layer (SEL), the medial (MPZ) and the lateral palisade zone (LPZ). The following areas were studied in F: the olfactory tubercle (TO), the dorsolateral nucleus accumbens (ACC), the medial part of the medial preoptic area (MPOA), the nucleus interstitialis striae terminalis ventralis (NISTV) and part of the 'striatal islands' in the caudate nucleus (CAUD). Serum LH, FSH and prolactin concentrations were determined by radio-immunoassay. In all experiments E₂B was given on day O at 0800-0900 h. On the basis of a time course study (day 0-6) the morning of day 3 was selected for an investigation of dose-effect relationships of E₂B (0.1-100 μg) on CA levels and turnover and serum LH, FSH and prolactin concentrations. Serum prolactin concentrations and DA turnover in the LPZ and TO were increased and serum LH and FSH concentrations and NA turnover in the SEL and MPOA were decreased in a dose-dependent manner by E₂B. LH concentrations correlated with DA turnover in the LPZ. Prolactin concentrations correlated with DA turnover in the ACC. LH and FSH concentrations correlated only after E₂B administration. It is concluded that 1) an inhibitory feedback effect of estrogen on LH secretion is exerted via DA terminals in the LPZ, 2) NA terminals in the MPOA may stimulate LH secretion, 3) a non-CA mechanism may regulate FSH secretion, and 4) DA terminals in the ACC may play a role in the control of prolactin secretion.