Chronic alcohol consumption induces an overproduction of NO by nNOS‐ and iNOS‐expressing myenteric neurons in the murine small intestine

Background  There are indications that alterations in the nitric oxide (NO) system of relaxation mediate gastrointestinal motor disturbances induced by chronic alcohol consumption (CAC). As CAC is known to inhibit the motility of the mouse small intestine, we investigated in this model if CAC affect...

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Veröffentlicht in:Neurogastroenterology and motility 2011-06, Vol.23 (6), p.e237-e248
Hauptverfasser: Bagyánszki, M., Torfs, P., Krecsmarik, M., Fekete, É., Adriaensen, D., Van Nassauw, L., Timmermans, J.‐P., Kroese, A. B. A.
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Sprache:eng
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Zusammenfassung:Background  There are indications that alterations in the nitric oxide (NO) system of relaxation mediate gastrointestinal motor disturbances induced by chronic alcohol consumption (CAC). As CAC is known to inhibit the motility of the mouse small intestine, we investigated in this model if CAC affects basal NO synthesis by myenteric neurons and which NOS isoforms are involved. Methods  The instantaneous NO synthesis of individual neurons was optically measured in whole‐mount preparations loaded with the NO synthesis indicator DAF‐FM, and the expression of nNOS, iNOS and eNOS was determined by immunohistochemistry. Key Results  The DAF‐FM recordings showed that CAC induced an increase in neuronal NO synthesis (absolute fluorescence: control 34 ± 12; CAC 140 ± 56; mean ± SD; P 
ISSN:1350-1925
1365-2982
DOI:10.1111/j.1365-2982.2011.01707.x