HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/1/R241    most recent 00498.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Hardwick, J. C. Articles by Powers, M. J. Search for Related Content PubMed PubMed Citation Articles by Hardwick, J. C. Articles by Powers, M. J.

INFLAMMATION AND CYTOKINES

Ionic mechanisms of histamine-induced responses in guinea pig intracardiac neurons

Biology Department, Ithaca College, Ithaca, New York

Submitted 8 July 2005 ; accepted in final form 30 August 2005

Histamine, released from mast cells, can modulate the activity of intrinsic neurons in the guinea pig cardiac plexus. The present study examined the ionic mechanisms underlying the histamine-induced responses in these cells. Histamine evokes a small membrane depolarization and an increase in neuronal excitability. Using intracellular voltage recording from individual intracardiac neurons, we were able to demonstrate that removal of extracellular sodium reduced the membrane depolarization, whereas inhibition of K⁺ channels by 1 mM Ba²⁺, 2 mM Cs⁺, or 5 mM tetraethylammonium had no effect. The depolarization was also not inhibited by either 10 µM Gd³⁺ or a reduced Cl^– solution. The histamine-induced increase in excitability was unaffected by K⁺ channel inhibitors; however, it was reduced by either blockage of voltage-gated Ca²⁺ channels with 200 µM Cd²⁺ or replacement of extracellular Ca²⁺ with Mg²⁺. Conversely, alterations in intracellular calcium with thapsigargin or caffeine did not inhibit the histamine-induced effects. However, in cells treated with both thapsigargin and caffeine to deplete internal calcium stores, the histamine-induced increase in excitability was decreased. Treatment with the phospholipase C inhibitor U73122 [GenBank] also prevented both the depolarization and the increase in excitability. From these data, we conclude that histamine, via activation of H₁ receptors, activates phospholipase C, which results in 1) the opening of a nonspecific cation channel, such as a transient receptor potential channel 4 or 5; and 2) in combination with either the influx of Ca²⁺ through voltage-gated channels or the release of internal calcium stores leads to an increase in excitability.

tetraethylammonium; phospholipase C; mast cells; H₁ receptor

This article has been cited by other articles:

				J. C. Hardwick, C. N. Baran, E. M. Southerland, and J. L. Ardell Remodeling of the guinea pig intrinsic cardiac plexus with chronic pressure overload Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R859 - R866. [Abstract] [Full Text] [PDF]

				J. D. Tompkins, Y. T. Lawrence, and R. L. Parsons Enhancement of Ih, but not inhibition of IM, is a key mechanism underlying the PACAP-induced increase in excitability of guinea pig intrinsic cardiac neurons Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2009; 297(1): R52 - R59. [Abstract] [Full Text] [PDF]

				J. C. Hardwick, E. M. Southerland, and J. L. Ardell Chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig cardiac plexus Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1926 - R1933. [Abstract] [Full Text] [PDF]

				J. Zhou, A. W. Lee, N. Devidze, Q. Zhang, L.-M. Kow, and D. W. Pfaff Histamine-Induced Excitatory Responses in Mouse Ventromedial Hypothalamic Neurons: Ionic Mechanisms and Estrogenic Regulation J Neurophysiol, December 1, 2007; 98(6): 3143 - 3152. [Abstract] [Full Text] [PDF]