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Articles in PresS, published online ahead of print August 21, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00141.2002
Submitted on April 11, 2002
Accepted on July 25, 2002
1 Department of Anatomy and Neurobiology, University of Vermont, Burlington, Vermont, USA
2 Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
3 Department of Anatomy and Neurobiology, University of Vermont, Burlington, Vermont, USA; Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: gmawe{at}zoo.uvm.edu.
PGE2 is a pro-inflammatory mediator that can influence many cell types. This study was conducted to determine whether PGE2 alters the electrical activity of distal colonic myenteric neurons because colitis is typically associated with altered motility, and changes in neural signaling may be involved. The electrical properties of intact myenteric neurons were evaluated with intracellular microelectrodes. Acute application of PGE2 elicited a prolonged depolarization in both AH and S neurons, with little effect on input resistance or electrical excitability. PGE2 effects were suppressed by TTX or neurokinin receptor antagonists, indicating that PGE2 acts directly and indirectly to depolarize colonic neurons. The PGE2-evoked depolarization was concentration-dependent (EC50 = ~3 µM) and was attenuated by the EP1/EP2 receptor antagonist, AH 6809. When preparations were maintained for 48 hours in the presence of the stable PGE2 analog, PGE2-ethanolamide (10 µM), neurons exhibited a significant membrane depolarization and enhanced excitability. These results suggest that PGE2 can play a role in altered motility in colitis by evoking changes in the electrical properties of myenteric neurons.
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