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Am J Physiol Gastrointest Liver Physiol 287: G274-G285, 2004. First published February 12, 2004; doi:10.1152/ajpgi.00472.2003
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NEUROREGULATION AND MOTILITY

Altered gene expression and increased bursting activity of colonic smooth muscle ATP-sensitive K+ channels in experimental colitis

Xiaochun Jin,1 Anna P. Malykhina,1 Florea Lupu,2 and Hamid I. Akbarali1

1Department of Physiology and 2Oklahoma Medical Research Foundation, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73034

Submitted 6 November 2003 ; accepted in final form 7 February 2004

The ATP-sensitive K+ channel (KATP) is a complex composed of an inwardly rectifying, pore-forming subunit (Kir 6.1 and Kir 6.2) and the sulfonylurea receptor (SUR1 and SUR2). In gastrointestinal smooth muscle, these channels are important in regulating cell excitability. We examined the molecular composition of the KATP channel in mouse colonic smooth muscle and determined its activity in the pathophysiological setting of experimental colitis. Following 7 days of dextran sulfate sodium (DSS) treatment in drinking water, colonic inflammation was scored by histology and physical signs. In whole cell recordings, levcromakalim-induced currents were significantly larger in inflamed cells. In cell-attached patch recordings of single-channel events, levcromakalim enhanced the bursting duration in inflamed cells. The single-channel conductance of ~42 pS was not altered with inflammation. mRNA for both Kir 6.1 and 6.2 were detected by RT-PCR. Kir 6.1 was localized to the plasma membrane, whereas Kir 6.2 was mainly detected in the cytosol by immunohistochemistry. Quantitative PCR showed that Kir 6.1 gene expression was upregulated by almost 22-fold, whereas SUR2B was downregulated by threefold after inflammation. Thus decreased motility of the colon during inflammation may be associated with changes in the transcriptional regulation of Kir 6.1 and SUR2B gene expression.

sulphonylurea receptor; inflammation; dextran sulfate; real-time PCR; voltage clamp


Address for reprint requests and other correspondence: H. I. Akbarali, Dept. of Physiology, Univ. of Oklahoma Health Science Center 940 Stanton L. Young Blvd., Oklahoma City, OK 73104 (E-mail: hamid-akbarali{at}ouhsc.edu).




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