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NEUROREGULATION AND MOTILITY

Stimulation of neurons in rat ARC inhibits gastric acid secretion via hypothalamic CRF1/2- and NPY-Y₁ receptors

Division Gastroenterology and Endocrinology, Departments of ¹Internal Medicine and ²Molecular Neuroscience, Institute of Anatomy and Cell Biology, Philipps Universität Marburg, 35033 Marburg; and ³Divisions of Hepatology and Gastroenterology and Psychosomatic Medicine and Psychotherapy, Department of Medicine, Charité, Campus Virchow-Klinikum, Humboldt Universität, 13353 Berlin, Germany

Submitted 18 March 2003 ; accepted in final form 30 June 2003

Neuropeptide Y (NPY) neuronal projections from the arcuate nucleus (ARC) have been proposed to target corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus (PVN) as part of the ARC-PVN axis. The existence of a positive feedback loop involving CRF receptors in the PVN has been suggested. Exogenous NPY and CRF in the PVN have been shown to inhibit gastric acid secretion. Recently, we have demonstrated that activation of ARC neurons inhibits gastric acid secretion via vagal pathways. To what extent NPY- and CRF-mediated mechanisms in the PVN contribute to the CNS modulation of gastric acid secretion is still an open question. In the present study, we performed consecutive bilateral microinjections of antagonists to NPY receptor subtypes Y₁ and Y₂ and to CRF1/2 receptors in the PVN and of the excitatory amino acid kainate in the ARC to assess the role of NPY- and CRF-mediated mechanisms in the kainate-induced effects on gastric acid secretion. Gastric acid secretion was measured at the basal condition and during pentagastrin (16 µg/kg body wt) stimulation. Microinjection of vehicle in the PVN and kainate in the ARC decreased gastric acid secretion. Microinjection of the specific NPY-Y₁ receptor antagonist BIBP-3226 (200 pmol) and the nonspecific CRF1/2 antagonist astressin (30 pmol) in the PVN abolished the inhibitory effect of neuronal activation in the ARC by kainate on gastric acid secretion. The CRF antagonist astressin was more effective. Pretreatment with the NPY-Y₂ receptor antagonist BIIE-0246 (120 pmol) in the PVN had no significant effect. Our results indicate that activation of neurons in the ARC inhibits gastric acid secretion via CRF1/2 and NPY-Y₁ receptor-mediated pathways in the PVN.

brain-gut interaction; arcuate nucleus; paraventricular nucleus of the hypothalamus; neuropeptide Y; corticotropin-releasing factor