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Neurogastroenterol Motil. 2010 May;22(5):e162-70. doi: 10.1111/j.1365-2982.2009.01467.x. Epub 2010 Feb 1.

Increased colonic motility in a rat model of irritable bowel syndrome is associated with up-regulation of L-type calcium channels in colonic smooth muscle cells.

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School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.



This paper aimed to investigate the relationship between up-regulation of L-type calcium channels and altered motility disorder in a rat model of irritable bowel syndrome (IBS).


Male Sprague-Dawley rats were subjected to neonatal maternal separation (NMS) from postnatal day 2-14 or normal handling (NH), and used when weighted 250-300 g. Colonic smooth muscle contractions was studied in an organ bath system. L-type Ca(2+) channel alpha(1c) subunit expression in smooth muscles from rat colon were studied by immunofluorescence and Western blotting analysis. The intracellular calcium concentration ([Ca(2+)](i)) of enzymatically isolated single colonic smooth muscle cell was studied with laser confocal fluorescent microscopy.


The fecal pellets during 1 h water avoidance stress (WAS) were significantly increased; the amplitude of spontaneous contractions and contractions induced by Bay K 8644 (10 nM-1 microM), KCl (10-60 mM) and ACh (100 nM-10 microM) were significantly increased in NMS rats, when comparing with that of NH rats. [Ca(2+)]i induced by Bay K 8644 (1 microM), KCl (40 mM), and ACh (10 microM) significantly increased in muscle cells of NMS rats than NH rats. Further, alpha(1c) protein expression was significantly up-regulated in colonic smooth muscle of NMS rats than NH rats.


These results suggest that NMS lead to up-regulation of L-type Ca(2+) channels expression in the colon, which contributes to the colonic motility disorder. Our findings provide direct evidence to help understanding the underlying mechanism of chronic stress-induced colonic motility disorder in IBS.

[Indexed for MEDLINE]

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