Neural pathway of estrogen receptor a expression during stress-induced suppression of luteinizing hormone secretion
Issue Date
6-2009
Abstract
This review article describes the role and regulatory mechanism of estrogen receptor a (ERa) expression in specific brain areas to give further insights on the brain mechanism of estrogen-enhancement of suppression of luteinizing hormone (LH) secretion by certain stressors in female rats. It shows that, (1) certain metabolic i.e. fasting, 2DG-induced glucoprivation, and physical (immobilization) stress induced an increase in ERa expression in specific hypothalamic and brainstem areas, (2) the increased number of ERa in the hypothalamic paraventricular nucleus (PVN) and A1 and/or A 2 brainstem region(s) during fasting and glucoprivation is required for estrogen potentiation of LH suppression by these stressors, (3) vagal input is needed for the induction of ERa expression in the brainstem A2 region that may trigger the neural pathway of LH suppression during fasting, (4) brainstem A, and/or A2 catecholaminergic inputs to the PVN stimulates the increase in ERa in the PVN during glucoprivation and fasting, respectively, so that estrogen can enhance the sensitivity of the PVN corticotropin releasing hormone (CRH) neurons to the catecholaminergic stimulus needed for the suppression of LH secretion, (5) activation of the A2 catecholaminergic input to the PVN is a common pathway utilized by certain metabolic and physical stressors for the induction of neural ERa expression and suppression of pulsatile LH secretion.
Source or Periodical Title
Philippine Journal of Veterinary Medicine
ISSN
317705
Volume
46
Issue
1
Page
61-72
Document Type
Article
College
College of Veterinary Medicine (CVM)
Language
English
Subject
Estrogen, Estrogen receptor, Fasting, Glucoprivation, Stress
Recommended Citation
Neural pathway of estrogen receptor alpha expression during stress-induced suppression of luteinizing hormone secretion. (2009). Philippine Journal of Veterinary Medicine (Philippines), 46(1), 61–72
Digital Copy
None