Glucoprivation increases estrogen receptor α immunoreactivity in the brain catecholaminergic neurons in ovariectomized rats

Estrogen-dependent enhancement of glucoprivic-induced luteinizing hormone (LH) suppression is hypothesized to be due to increased estrogen receptor a (ER alpha)-immunoreactive (ir) cells in specific brain nuclei in a manner similar to fasting. ER alpha expression in various brain areas was determined in ovariectomized rats after systemic 2-deoxy-D-glucose (2DG)-induced glucoprivation. Expression of ER alpha in catecholaminergic neurons in the lower brainstem was also examined. ER alpha -ir cells increased in hypothalamic paraventricular and periventricular nuclei, and A1 and A2 regions of the brainstem 1 h after 2DG injection. The percentage of ER alpha in the tyrosine hydroxylase (TH)- and dopamine-betaL-hydroxylase (DBH)-ir neurons was higher in A1 and A2 regions of 2DG-treated rats, but the number of TH- and DBH-ir cells did not change. Thus, 2DG induces ERa expression in specific brain nuclei and expression of ERa in catecholaminergic neurons of the brainstem indicates a role for estrogen in activating those neurons projecting to the hypothalamic paraventricular nucleus to suppress LH secretion during glucoprivation. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.