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AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 4 1034-R1039, Copyright © 1995 by American Physiological Society
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C. D. Sladek, K. Y. Fisher, H. E. Sidorowicz and J. R. Mathiasen
Department of Physiology, Finch University of Health Sciences, Chicago Medical School, Illinois 60064, USA.
The role of synaptic input to the vasopressin neurons in hypertonicity-induced increase in vasopressin mRNA content was evaluated. Synaptic connection with the anterior hypothalamus is required for hypertonicity to increase vasopressin release. However, the potential for other mechanisms to induce the increase in vasopressin mRNA content is suggested by the fact that hypertonicity induces depolarization of supraoptic neurons independently of synaptic input. Explants of the hypothalamoneurohypophysial system were used to study the effect of depolarization and hypertonicity in the presence and absence of nonspecific synaptic blockade by 15 mM MgSO4 or blockade of excitatory amino acid receptors with kynurenic acid. Vasopressin release and mRNA content were increased by depolarization with 40 mM KCl and by exposure to hypertonicity (P < 0.05). Basal and osmotically stimulated vasopressin release was decreased by MgSO4 and by kynurenic acid. Both agents prevented the hypertonicity-induced increase in vasopressin mRNA content. Thus either synaptic input or increased VP release is required for hypertonicity to increase vasopressin mRNA, and excitatory amino acids are implicated in this response.
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