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J Neurophysiol 83: 1809-1816, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 83 No. 4 April 2000, pp. 1809-1816
Copyright ©2000 by the American Physiological Society

Histamine H2 Receptor Activated Chloride Conductance in Myenteric Neurons From Guinea Pig Small Intestine

Alexander M. Starodub and Jackie D. Wood

Department of Physiology, College of Medicine and Public Health, Ohio State University, Columbus, Ohio 43210-1218

Starodub, Alexander M. and Jackie D. Wood. Histamine H2 Receptor Activated Chloride Conductance in Myenteric Neurons From Guinea Pig Small Intestine. J. Neurophysiol. 83: 1809-1816, 2000. Whole cell perforated patch-clamp methods were used to investigate ionic mechanisms underlying histamine-evoked excitatory responses in small intestinal AH-type myenteric neurons. When physiological concentrations of Na+, Ca2+, and Cl- were in the bathing medium, application of histamine significantly increased total conductance as determined by stepping to 50 mV from a holding potential of -30 mV. The current reversed at a membrane potential of -30 ± 5 (SE) mV and current-voltage relations exhibited outward rectification. The reversal potential for the histamine-activated current was unchanged by removal of Na+ and Ca2+ from the bathing medium. Reduction of Cl- from 155 mM to 55 mM suppressed the current when the neurons were in solutions with depleted Na+ and Ca2+. Current-voltage curves in solutions with reduced Cl- were linear and the reversal potential was changed from -30 ± 5 mV to 7 ± 4 mV. Niflumic acid, but not anthracene-9-carboxylic acid (9-AC) nor 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), suppressed the histamine-activated current. A membrane permeable analogue of cAMP evoked currents similar to those activated by histamine. A selective histamine H2 receptor agonist (dimaprit) mimicked the action of histamine and a selective histamine H2 receptor antagonist (cimetidine) blocked the conductance increase evoked by histamine. A selective adenosine A1 receptor agonist (CCPA) reduced the histamine-activated current and a selective adenosine A1 receptor antagonist (CPT) reversed the inhibitory action. The results suggest that histamine acts at histamine H2 receptors to increase Cl- conductance in AH-type enteric neurons. Cyclic AMP appears to be a second messenger in the signal transduction process. Results with a selective adenosine A1 receptor agonist and antagonist add to existing evidence for co-coupling of inhibitory adenosine A1 receptors and histamine H2 receptors to adenylate cyclase in AH-type enteric neurons.




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