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J Neurophysiol (May 21, 2003). doi:10.1152/jn.01079.2002
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Submitted on December 2, 2002
Accepted on May 20, 2003

Muscarinic and nicotinic ACh receptor activation differentially mobilize Ca2+ in rat intracardiac neurons

Friederike Beker1, Martin Weber1, Rainer H. Fink2, and David J. Adams3*

1 Institut fur Physiologie und Pathophysiologie, Ruprecht-Karls-Universitat Heidelberg, Heidelberg, Germany; School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia
2 Institut fur Physiologie und Pathophysiologie, Ruprecht-Karls-Universitat Heidelberg, Heidelberg, Germany
3 School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia

* To whom correspondence should be addressed. E-mail: dadams{at}uq.edu.au.

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, which 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 upon mAChR activation and with rapid inward currents following 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.




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