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Pathways involved in gut mucosal barrier dysfunction induced in adult rats by maternal deprivation: corticotrophin-releasing factor and nerve growth factor interplay

Barreau, Frederick and Cartier, Christel and Leveque, Mathilde and Ferrier, Laurent and Moriez, Raphael and Laroute, Valerie and Rosztoczy, Andras and Fioramonti, Jean and Bueno, Lionel Pathways involved in gut mucosal barrier dysfunction induced in adult rats by maternal deprivation: corticotrophin-releasing factor and nerve growth factor interplay. (2007) The Journal of Physiology, vol. 5 (n° 1). pp. 347-356. ISSN 0022-3751

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Official URL: http://jp.physoc.org/cgi/reprint/580/1/347

Abstract

Neonatal maternal deprivation (NMD) increases gut paracellular permeability (GPP) through mast cells and nerve growth factor (NGF), and modifies corticotrophin-releasing factor (CRF) and corticosterone levels. CRF, corticosterone and mast cells are involved in stress-induced mucosal barrier impairment. Consequently, this study aimed to specify whether corticosteronaemia and colonic expression of both preproCRF and CRF are modified by NMD, and to determine if altered expression may participate in the elevated GPP in connection with NGF and mast cells. Male Wistar rat pups were either separated from postnatal days 2–14, or left undisturbed with their dam. At 12 weeks of age, adult rats were treated with mifepristone (an antagonist of corticoid receptors), {alpha}-helical CRF(9-41) (a non-specific CRF receptor antagonist), or SSR-125543 (CRF-R1 receptor antagonist). We also determined corticosteronaemia and both colonic preproCRF and CRF expression. Then, control rats were treated by CRF, doxantrazole (mast cell stabilizer), BRX-537A (a mast cell activator) and anti-NGF antibody. NMD did not modify colonic CRF level but increased colonic preproCRF expression and corticosteronaemia. Peripheral CRF, via CRF-R1 receptor, but not corticosterone, was involved in the elevated GPP observed in these rats, through a mast-cell-mediated mechanism, since the increase of GPP induced by exogenous CRF was abolished by doxantrazole. Anti-NGF antibody treatment also reduced the elevated GPP induced by CRF or BRX-537A. CRF acts through CRF-R1 receptors to stimulate NGF release from mast cells, which participates in the elevated GPP observed in NMD adult rats. This suggests that early traumatic experience induced neuro-endocrine dysfunction, involved in alterations of gut mucosal barrier.

Item Type:Article
Additional Information:Thanks to Cambridge University Press and Blackwell. The definitive version is available at www.blackwell-synergy.com The original PDF of the article can be found at The Journal of Physiology website : http://jp.physoc.org/cgi/reprint/580/1/347
Audience (journal):International peer-reviewed journal
Uncontrolled Keywords:
Institution:French research institutions > Institut National de la Recherche Agronomique - INRA
Université de Toulouse > Ecole Nationale Vétérinaire de Toulouse - ENVT
Other partners > University of Szeged (HUNGARY)
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Deposited By:Mathieu Andro

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