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: 96/5/2479    most recent 00093.2006v1 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 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 Yang, Q. Articles by Ruiz-Velasco, V. Search for Related Content PubMed PubMed Citation Articles by Yang, Q. Articles by Ruiz-Velasco, V.

M₁ and M₂ Muscarinic Acetylcholine Receptor Subtypes Mediate Ca²⁺ Channel Current Inhibition in Rat Sympathetic Stellate Ganglion Neurons

¹Departments of Anesthesiology and ²Medicine, Penn State College of Medicine, Hershey, Pennsylvania; and ³Laboratory of Molecular Physiology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland

Submitted 27 January 2006; accepted in final form 4 August 2006

Muscarinic acetylcholine receptors (mAChRs) are known to mediate the acetylcholine inhibition of Ca²⁺ channels in central and peripheral neurons. Stellate ganglion (SG) neurons provide the main sympathetic input to the heart and contribute to the regulation of heart rate and myocardial contractility. Little information is available regarding mAChR regulation of Ca²⁺ channels in SG neurons. The purpose of this study was to identify the mAChR subtypes that modulate Ca²⁺ channel currents in rat SG neurons innervating heart muscle. Accordingly, the modulation of Ca²⁺ channel currents by the muscarinic cholinergic agonist, oxotremorine-methiodide (Oxo-M), and mAChR blockers was examined. Oxo-M–mediated mAChR stimulation led to inhibition of Ca²⁺ currents through voltage-dependent (VD) and voltage-independent (VI) pathways. Pre-exposure of SG neurons to the M₁ receptor blocker, M₁-toxin, resulted in VD inhibition of Ca²⁺ currents after Oxo-M application. On the other hand, VI modulation of Ca²⁺ currents was observed after pretreatment of cells with methoctramine (M₂ mAChR blocker). The Oxo-M–mediated inhibition was nearly eliminated in the presence of both M₁ and M₂ mAChR blockers but was unaltered when SG neurons were exposed to the M₄ mAChR toxin, M₄-toxin. Finally, the results from single-cell RT-PCR and immunofluorescence assays indicated that M₁ and M₂ receptors are expressed and located on the surface of SG neurons. Overall, the results indicate that SG neurons that innervate cardiac muscle express M₁ and M₂ mAChR, and activation of these receptors leads to inhibition of Ca²⁺ channel currents through VI and VD pathways, respectively.

This article has been cited by other articles:

				N. Da Silva, C. E. Herron, K. Stevens, C. A. B. Jollimore, S. Barnes, and M. E. M. Kelly Metabotropic Receptor-Activated Calcium Increases and Store-Operated Calcium Influx in Mouse Muller Cells Invest. Ophthalmol. Vis. Sci., July 1, 2008; 49(7): 3065 - 3073. [Abstract] [Full Text] [PDF]