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: 90/3/1956    most recent 01079.2002v1 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 ISI 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 ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Beker, F. Articles by Adams, D. J. Search for Related Content PubMed PubMed Citation Articles by Beker, F. Articles by Adams, D. J.

Muscarinic and Nicotinic ACh Receptor Activation Differentially Mobilize Ca²⁺ in Rat Intracardiac Ganglion Neurons

¹ School of Biomedical Sciences, University of Queensland, Brisbane, Queeensland 4072, Australia; ² Institut für Physiologie und Pathophysiologie, Ruprecht-Karls-Universität Heidelberg, 69120 Heidelberg, Germany

Submitted 2 December 2002; accepted in final form 20 May 2003

The origin of intracellular Ca²⁺ concentration ([Ca²⁺]_i) transients stimulated by nicotinic (nAChR) and muscarinic (mAChR) receptor activation was investigated in fura-2-loaded neonatal rat intracardiac neurons. ACh evoked [Ca²⁺]_i increases that were reduced to 60% of control in the presence of either atropine (1 µM) or mecamylamine (3 µM) and to <20% in the presence of both antagonists. Removal of external Ca²⁺ reduced ACh-induced responses to 58% of control, which was unchanged in the presence of mecamylamine but reduced to 5% of control by atropine. The nAChR-induced [Ca²⁺]_i response was reduced to 50% by 10 µM ryanodine, whereas the mAChR-induced response was unaffected by ryanodine, suggesting that Ca²⁺ release from ryanodine-sensitive Ca²⁺ stores may only contribute to the nAChR-induced [Ca²⁺]_i responses. Perforated-patch whole cell recording at –60 mV shows that the rise in [Ca²⁺]_i is concomitant with slow outward currents on mAChR activation and with rapid inward currents after nAChR activation. In conclusion, different signaling pathways mediate the rise in [Ca²⁺]_i and membrane currents evoked by ACh binding to nicotinic and muscarinic receptors in rat intracardiac neurons.

This article has been cited by other articles:

				J. D. Tompkins, J. L. Ardell, D. B. Hoover, and R. L. Parsons Neurally released pituitary adenylate cyclase-activating polypeptide enhances guinea pig intrinsic cardiac neurone excitability J. Physiol., July 1, 2007; 582(1): 87 - 93. [Abstract] [Full Text] [PDF]

				W. I. DeHaven and J. Cuevas VPAC Receptor Modulation of Neuroexcitability in Intracardiac Neurons: DEPENDENCE ON INTRACELLULAR CALCIUM MOBILIZATION AND SYNERGISTIC ENHANCEMENT BY PAC1 RECEPTOR ACTIVATION J. Biol. Chem., September 24, 2004; 279(39): 40609 - 40621. [Abstract] [Full Text] [PDF]