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Histamine H(2) receptor activated chloride conductance in myenteric neurons from guinea pig small intestine.
J Neurophysiol. 2000 Apr; 83(4):1809-16.JN

Abstract

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(+), Ca(2+), 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 Ca(2+) 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 Ca(2+). 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 H(2) receptor agonist (dimaprit) mimicked the action of histamine and a selective histamine H(2) receptor antagonist (cimetidine) blocked the conductance increase evoked by histamine. A selective adenosine A(1) receptor agonist (CCPA) reduced the histamine-activated current and a selective adenosine A(1) receptor antagonist (CPT) reversed the inhibitory action. The results suggest that histamine acts at histamine H(2) 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 A(1) receptor agonist and antagonist add to existing evidence for co-coupling of inhibitory adenosine A(1) receptors and histamine H(2) receptors to adenylate cyclase in AH-type enteric neurons.

Authors+Show Affiliations

Department of Physiology, College of Medicine and Public Health, Ohio State University, Columbus, Ohio 43210-1218, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10758093

Citation

Starodub, A M., and J D. Wood. "Histamine H(2) Receptor Activated Chloride Conductance in Myenteric Neurons From Guinea Pig Small Intestine." Journal of Neurophysiology, vol. 83, no. 4, 2000, pp. 1809-16.
Starodub AM, Wood JD. Histamine H(2) receptor activated chloride conductance in myenteric neurons from guinea pig small intestine. J Neurophysiol. 2000;83(4):1809-16.
Starodub, A. M., & Wood, J. D. (2000). Histamine H(2) receptor activated chloride conductance in myenteric neurons from guinea pig small intestine. Journal of Neurophysiology, 83(4), 1809-16.
Starodub AM, Wood JD. Histamine H(2) Receptor Activated Chloride Conductance in Myenteric Neurons From Guinea Pig Small Intestine. J Neurophysiol. 2000;83(4):1809-16. PubMed PMID: 10758093.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histamine H(2) receptor activated chloride conductance in myenteric neurons from guinea pig small intestine. AU - Starodub,A M, AU - Wood,J D, PY - 2000/4/12/pubmed PY - 2000/5/20/medline PY - 2000/4/12/entrez SP - 1809 EP - 16 JF - Journal of neurophysiology JO - J Neurophysiol VL - 83 IS - 4 N2 - 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(+), Ca(2+), 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 Ca(2+) 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 Ca(2+). 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 H(2) receptor agonist (dimaprit) mimicked the action of histamine and a selective histamine H(2) receptor antagonist (cimetidine) blocked the conductance increase evoked by histamine. A selective adenosine A(1) receptor agonist (CCPA) reduced the histamine-activated current and a selective adenosine A(1) receptor antagonist (CPT) reversed the inhibitory action. The results suggest that histamine acts at histamine H(2) 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 A(1) receptor agonist and antagonist add to existing evidence for co-coupling of inhibitory adenosine A(1) receptors and histamine H(2) receptors to adenylate cyclase in AH-type enteric neurons. SN - 0022-3077 UR - https://www.unboundmedicine.com/medline/citation/10758093/Histamine_H_2__receptor_activated_chloride_conductance_in_myenteric_neurons_from_guinea_pig_small_intestine_ DB - PRIME DP - Unbound Medicine ER -