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Morphological Substrate of the Catecholaminergic Input of the Vasopressin Neuronal System in Humans
Author(s) -
Dudás B.,
Semeniken K. R.,
Merchenthaler I.
Publication year - 2006
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2006.01487.x
Subject(s) - vasopressin , endocrinology , catecholaminergic , medicine , supraoptic nucleus , hypothalamus , biology , thirst , neuropeptide , chemistry , dopamine , receptor
It has been postulated that the stress response is associated with water balance via regulating vasopressin release. Nausea, surgical stress and insulin‐induced hypoglycaemia were shown to stimulate vasopressin secretion in humans. Increased vasopressin release in turn induces water resorption through the kidneys. Although the mechanism of the stress‐mediated vasopressin release is not entirely understood, it is generally accepted that catecholamines play a crucial role in influencing water balance by modulating the secretion of vasopressin. However, the morphological substrate of this modulation has not yet been established. The present study utilised double‐label immunohistochemistry to reveal putative juxtapositions between tyrosine hydroxylase (TH)‐immunoreactive (IR) catecholaminergic system and the vasopressin systems in the human hypothalamus. In the paraventricular and supraoptic nuclei, numerous vasopressin‐IR neurones received TH‐IR axon varicosities. Analysis of these juxtapositions with high magnification combined with oil immersion did not reveal any gaps between the contacted elements. In conclusion, the intimate associations between the TH‐IR and vasopressin‐IR elements may be functional synapses and may represent the morphological basis of vasopressin release modulated by stressors. Because certain vasopressin‐IR perikarya receive no detectable TH innervations, it is possible that additional mechanisms may participate in the stress‐influenced vasopressin release.

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