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Endocrinology Vol. 143, No. 2 456-466
Copyright © 2002 by The Endocrine Society


NEUROENDOCRINOLOGY

The Vasopressin Receptors Colocalize with Vasopressin in the Magnocellular Neurons of the Rat Supraoptic Nucleus and Are Modulated by Water Balance

Amandine Hurbin, Hélène Orcel, Gérard Alonso, Françoise Moos and Alain Rabié

Centre National de la Recherche Scientifique—Unité Mixte de Recherche 5101, Biologie des Neurones Endocrines, Centre de Pharmacologie-Endocrinologie, Montpellier F-34094, France

Address all correspondence and requests for reprints to: A. Rabié, CNRS-UMR 5101, CCIPE, 141 rue de la Cardonille, F-34094 Montpellier Cedex 5, France. E-mail: rabie{at}ccipe.montp.inserm.fr

Activity of the magnocellular neurons that synthesize vasopressin in the supraoptic and paraventricular nuclei of the hypothalamus is modulated by local release of the neuropeptide within the nuclei. V1a and V1b vasopressin receptor genes are expressed in these cells. The present study reports the localization of V1a and V1b receptors using multiple labeling immunocytochemistry. Both receptors are mainly located in vasopressinergic magnocellular neurons and colocalized with vasopressin in cytoplasmic vesicles dispersed throughout the cell. Possible functional modifications of the mRNA and protein levels of the V1a receptor, the major isoform, were also investigated by semiquantitative in situ hybridization and immunocytochemistry in rats submitted to reduced or increased water intake. V1a mRNA and receptor levels varied with water balance. V1a mRNA level dropped in rats submitted to high water intake. Conversely, dehydration up-regulated the V1a receptor content. These observations suggest that the pathways that regulate the expression of the genes encoding vasopressin and the V1a receptor are linked, which fits the present findings that the two partners are colocalized in cytoplasmic vesicles. Colocalization might explain how V1 autoreceptors are controlled by cell activity and/or local concentration of vasopressin (released locally by the neurons themselves), allowing fine adjustment of magnocellular neuron activity.




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