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Am J Physiol Gastrointest Liver Physiol (January 29, 2009). doi:10.1152/ajpgi.90511.2008
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Submitted on August 25, 2008
Revised on January 12, 2009
Accepted on January 14, 2009

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Xuelian Ma1, Yu-Kang Mao2, Bingxian Wang, Jan D. Huizinga3, John Bienenstock4, and Wolfgang A Kunze1*

1 The Brain-Body Institute
2 Mcmaster University
3 McMaster University
4 McMaster University, St. Joseph's Healthcare Hamilton

* To whom correspondence should be addressed. E-mail: kunzew{at}mcmaster.ca.

Lactobacillus species ingestion can decrease autonomic responses and spinal fibre discharge to nociceptive colorectal distension (CRD), even in the absence of inflammation. The present study aimed to determine if dorsal root ganglion (DRG) somas could be a locus where the anti-nociceptive probiotic may have an effect. Healthy rats were fed with Lactobacillus reuteri, or vehicle control for 9 days whereupon they were anaesthetised and intermittent distal colonic CRD at 80 mmHg distension was either performed for 1 hr, or not. The animals were immediately sacrificed and patch clamp recordings taken after isolation and overnight culture from those DRG that projected to the distal colon. CRD increased both the threshold for action potential generation and the number of spikes discharged during a standard depolarising test stimulus, and this effect was blocked by prior probiotic ingestion. The increase in excitability was paralleled by an increase in DRG soma size and capacitance which were not altered by Lactobacillus reuteriingestion. CRD did not increase tissue weight or myeloperoxidase activity. We suggest that the effects of CRD may have been caused by activity dependent neurotransmission between DRG somas. CRD evoked increases in action potential upstroke speed which suggests that it may also have led to augmentation of sodium channel conductances. Probiotic ingestion may have interfered with this hypothetical mechanism since it blocked effect of CRD on the action potential.







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