Abstract

The precise sites and mechanisms by which gonadal steroids influence the activity of neuroendocrine cells controlling pituitary hormone secretion are poorly understood. The present study has determined the distribution of estrogen receptor (ER)-immunoreactive cells in the monkey hypothalamus and examined whether ERs are expressed by luteinising hormone-releasing hormone (LHRH)-and/or dopamine-containing neurones. The distribution of ER-immunoreactive cells was determined in ovariectomised (n = 2) and estrogen plus progesterone-treated (n = 2) cynomolgus macaques and in a single ovariectomised African green monkey. Large numbers of cells immunoreactive for the ER were detected in the preoptic area, bed nucleus of the stria terminalis, periventricular area and ventromedial and arcuate nuclei of all monkeys irrespective of the steroid status. Smaller numbers of ER-immunoreactive cells were found in the paraventricular, but not supraoptic nucleus. Double-labeling experiments in sections from all 5 monkeys revealed that none of the 432 LHRH neurons examined possessed detectable ER immunoreactivity. Neurones stained for tyrosine hydroxylase (TH) were identified in the A11, A12, and A14 cell groups and, although A11 and A12 neurones were intermingled amongst and found adjacent to ER-immunoreactive cells, none of the 1,652 TH-immunoreactive cells examined contained ER immunoreactivity. These results show that ER-immunoreactive cells in the monkey hypothalamus are distributed in a manner similar to that observed in other mammalian species although not all brain regions reported to contain progesterone receptors (PRs) in these species of monkey were found to express ERs. The double-labelling experiments provide further evidence that LHRH neurones do not possess ERs and indicate that, as in other species, estrogen influences on primate LHRH neurones are indirect and/or non-genomic in nature. Unlike the rat and sheep, no evidence was found for ER immunoreactivity in hypothalamic dopaminergic neurones of the monkey. The discrepancy in ER and reported PR receptor localisation within specific hypothalamic nuclei as well as in dopaminergic neurones raises the possibility that not all PR-containing cells may express ERs in the primate hypothalamus.

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