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Am J Physiol Gastrointest Liver Physiol 281: G1203-G1213, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 5, G1203-G1213, November 2001

Colitis induces CRF expression in hypothalamic magnocellular neurons and blunts CRF gene response to stress in rats

Adelheid E. Kresse1, Mulugeta Million1, Esteban Saperas2, and Yvette Taché1

1 CURE: Digestive Diseases Research Center, Veterans Affairs Greater Los Angeles Healthcare System, Department of Medicine, Digestive Diseases Division and Brain Research Institute, School of Medicine, University of California, Los Angeles, California 90073; and 2 Digestive System Research Unit, Hospital General Vall d'Hebron, Autonomous University of Barcelona, 08035 Barcelona, Spain

We investigated hypothalamic neuronal corticotropin-releasing factor (CRF) gene expression changes in response to visceral inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNB) and acute stress. Seven days after TNB, rats were subjected to water-avoidance stress (WAS) or restraint for 30 min and euthanized. Hypothalamic CRF primary transcripts (heteronuclear RNA, hnRNA) and CRF and arginine vasopressin (AVP) mRNAs were assessed by in situ hybridization. Antisense 35S-labeled cRNA probes against CRF mRNA intronic and exonic sequences and an oligonucleotide probe against the AVP mRNA were used. TNB induced macroscopic lesions and a fivefold elevation in myeloperoxidase activity in the colon. Colitis increased CRF hnRNA and mRNA signals in the magnocellular part of the paraventricular nucleus of the hypothalamus (PVN) and supraoptic neurons, whereas AVP mRNA was not altered. Colitis did not modify CRF hnRNA signal in the parvocellular part of the PVN (pPVN), plasma corticosterone, and serum osmolarity levels. However, CRF hnRNA expression in the pPVN and the rise in corticosterone and defecation induced by WAS or restraint were blunted in colitic rats. These data show that colitis upregulates CRF gene synthesis in magnocellular hypothalamic neurons but dampens CRF gene transcription in the pPVN and plasma corticosterone responses to environmental acute stressors.

2,4,6-trinitrobenzenesulfonic acid; arginine vasopressin gene expression; supraoptic nucleus; osmolarity; heteronuclear corticotropin-releasing factor gene expression; defecation; food intake


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