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Department of Anatomy (E.H., I.K., T.H., Zs.L.), Albert Szent-Györgyi Medical University, 6724 Szeged, Hungary; and The Women’s Health Research Institute (P.S., I.M.), Wyeth-Ayerst Research, Radnor, Pennsylvania 19087
Address all correspondence and requests for reprints to: Istvan Merchenthaler, M.D., D.Sc., Women’s Health Research Institute, Wyeth-Ayerst Research, 1456 King of Prussia Road, Radnor, Pennsylvania 19087. E-mail: merchei{at}war.wyeth.com
The regulatory actions of estrogen on magnocellular oxytocin (OT) and
vasopressin (VP) neurons of the paraventricular (PVN) and supraoptic
(SON) nuclei are well documented. To date it is still debated whether
the effect of estrogens is exerted directly or mediated by
estrogen-sensitive interneurons. Previous immunocytochemical (ICC) and
in situ hybridization (ISH) studies detected either low
levels or absence of the classical estrogen receptor (ER-
) in the
PVN and the SON of the rat. The present experiments using a combined
ICC and ISH method were undertaken to examine the expression of the
recently cloned beta form of ER (ER-ß) in OT- and VP-immunoreactive
(IR) neuronal systems of the rat hypothalamus. The results demonstrate
that the highest cellular levels of ER-ß messenger RNA (mRNA) in
OT-IR neurons can be visualized in the caudal portion of the PVN and in
an area ventro-medial to the central core of VP-IR cells. These neurons
were previously shown to project caudally to the brain stem and the
spinal cord to regulate autonomic functions. In addition, the whole
rostro-caudal extent of the PVN and the SON contained OT-IR neurons
that coexpressed variable levels of ER-ß mRNA. Similarly, the
presence of ER-ß mRNA was seen in a large population of VP-IR
paraventricular and supraoptic neurons. In the SON, somewhat stronger
hybridization signal was detected in VP-IR neurons as compared with
OT-IR neurons.
Together, these findings provide strong support for the concept that the functions of OT- and VP-IR neurons in the PVN and the SON are regulated directly by estrogen and that the genomic effects of estrogens are mediated by ER-ß.
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