Alterations in the central vasopressin and oxytocin axis after lesion of a brain osmotic sensory region

Alterations in the central vasopressin and oxytocin axis after lesion of a brain osmotic sensory region

Autor Oliveira, G. R. Google Scholar
Franci, C. R. Google Scholar
Rodovalho, G. V. Google Scholar
Franci, JAA Google Scholar
Morris, M. Google Scholar
Rocha, MJA Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Wright State Univ
Resumo The anteroventral region of the third ventricle (AV3V) is critical in mediating osmotic sensitivity. AV3V lesions increase plasma osmolality and block osmotic-induced vasopressin (VP) and oxytocin (OT) secretion. the aim was to evaluate the effects of AV3V lesions on neurosecretion under control/water replete conditions and after 48 h dehydration. the focus was on central peptidergic changes with measurement of OT and VP content in the hypothalamic paraventricular (PVN) and supraoptic (OT) regions and the posterior pituitary. AV3V-lesioned rats exhibited an elevated plasma osmolality and higher OT content in SON and PVN. There was an increase in VP content in PVN, but no change in SON. As predicted, the plasma peptide response to dehydration was absent in lesioned animals. However, dehydration produced depletion in posterior pituitary VP in lesioned animals with no change in OT. No changes in nuclear VP and OT levels were seen after dehydration. These results demonstrate that AV3V lesions alter the VP and OT neurosecretory system, seen as a blockade of osmotic-induced release and an increase in basal nuclear peptide content. the data indicate that interruption of the osmotic sensory system affects the central neurosecretory axis, resulting in a backup in content and likely changes in synthesis and processing. (C) 2004 Elsevier Inc. All rights reserved.
Palavra-chave dehydration
Idioma Inglês
Data de publicação 2004-07-15
Publicado em Brain Research Bulletin. Oxford: Pergamon-Elsevier B.V., v. 63, n. 6, p. 515-520, 2004.
ISSN 0361-9230 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 515-520
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000222923200010
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