Type II glucocorticoid receptors in the ovine hypothalamus: distribution, influence of estrogen and absence of co-localization with GnRH.

There is a strong association between the stress-induced increase in cortisol secretion and perturbation of the neuroendocrine reproductive axis. Previous studies implicate a neural target for glucocorticoids and it is possible that cortisol may act directly on gonadotropin releasing hormone (GnRH) neurons and, thus, luteinizing hormone release, through type II glucocorticoid receptors (GRs). In this study we investigated the effect of estradiol on GR immunoreactivity and determined whether GnRH neurons contain GRs. GRs were dispersed throughout most diencephalic structures but were most concentrated within the medial preoptic area and arcuate nucleus. GR cell numbers were significantly higher in these two areas in ewes pre-treated only with progesterone compared to ewes pre-treated with estradiol plus progesterone; there was no variation in the paraventricular nucleus between groups. No colocalization between GnRH and GRs was observed at any level of the brain. These results suggest that estrogen may down-regulate GRs and glucocorticoids do not act directly on GnRH neurons in the ewe.