Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis.

Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis. Research Abstract Details 

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Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis. Abstract Text:

Thomas Wultsch,Evelin Painsipp,Anaid Shahbazian,Martina Mitrovic,Martin Edelsbrunner,Michel Lazdunski,Rainer Waldmann,Peter Holzer,Thomas Wultsch,Evelin Painsipp,Anaid Shahbazian,Martina Mitrovic,Martin Edelsbrunner,Michel Lazdunski,Rainer Waldmann,Peter Holzer,Thomas Wultsch,Evelin Painsipp,Anaid Shahbazian,Martina Mitrovic,Martin Edelsbrunner,Michel Lazdunski,Rainer Waldmann,Peter Holzer,

Gastric acid challenge of the rat and mouse stomach is signalled to the brainstem as revealed by expression of c-Fos. The molecular sensors relevant to the detection of gastric mucosal acidosis are not known. Since the acid-sensing ion channels ASIC2 and ASIC3 are expressed by primary afferent neurons, we examined whether knockout of the ASIC2 or ASIC3 gene modifies afferent signalling of a gastric acid insult in the normal and inflamed stomach. The stomach of conscious mice (C57BL/6) was challenged with intragastric HCl; two hours later the activation of neurons in the nucleus tractus solitarii (NTS) of the brainstem was visualized by c-Fos immunocytochemistry. Mild gastritis was induced by addition of iodoacetamide (0.1%) to the drinking water for 7 days. Exposure of the gastric mucosa to HCl (0.25M) caused a 3-fold increase in the number of c-Fos-positive neurons in the NTS. This afferent input to the NTS remained unchanged by ASIC3 knockout, whereas ASIC2 knockout augmented the c-Fos response to gastric HCl challenge by 33% (P<0.01). Pretreatment of wild-type mice with iodoacetamide induced mild gastritis, as revealed by increased myeloperoxidase activity, and enhanced the number of NTS neurons responding to gastric HCl challenge by 41% (P<0.01). This gastric acid hyperresponsiveness was absent in ASIC3 knockout mice but fully preserved in ASIC2 knockout mice. The current data indicate that ASIC3 plays a major role in the acid hyperresponsiveness associated with experimental gastritis. In contrast, ASIC2 appears to dampen acid-evoked input from the stomach to the NTS.

Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis. Publishing Authors By Initials

T Wultsch,E Painsipp,A Shahbazian,M Mitrovic,M Edelsbrunner,M Lazdunski,R Waldmann,P Holzer,T Wultsch,E Painsipp,A Shahbazian,M Mitrovic,M Edelsbrunner,M Lazdunski,R Waldmann,P Holzer,T Wultsch,E Painsipp,A Shahbazian,M Mitrovic,M Edelsbrunner,M Lazdunski,R Waldmann,P Holzer,

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Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Pain

VOLUME: 134

Page Numbers: 245-53

Journal Abbreviation: Pain

ISSN: 1872-6623

DAY: 24

MONTH: 05

YEAR: 2007

Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis. Information

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LANGUAGE: eng

NlmUniqueID: 7508686

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AFFILIATION: Research Unit of Translational Neurogastroenterology, Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Universitätsplatz 4, A-8010 Graz, Austria.

Country: Netherlands

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MEDLINETA: Pain

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