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

Abstract:

:Estrogen-dependent enhancement of glucoprivic-induced luteinizing hormone (LH) suppression is hypothesized to be due to increased estrogen receptor alpha (ERalpha)-immunoreactive (ir) cells in specific brain nuclei in a manner similar to fasting. ERalpha expression in various brain areas was determined in ovariectomized rats after systemic 2-deoxy-D-glucose (2DG)-induced glucoprivation. Expression of ERalpha in catecholaminergic neurons in the lower brainstem was also examined. ERalpha-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 ERalpha in the tyrosine hydroxylase (TH)- and dopamine-beta-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 ERalpha expression in specific brain nuclei and expression of ERalpha 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.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Reyes BA,Estacio MA,I'Anson H,Tsukamura H,Maeda KI

doi

10.1016/s0304-3940(01)01490-2

keywords:

subject

Has Abstract

pub_date

2001-02-16 00:00:00

pages

109-12

issue

1-2

eissn

0304-3940

issn

1872-7972

pii

S0304394001014902

journal_volume

299

pub_type

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