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J Neurophysiol 90: 613-621, 2003. First published April 30, 2003; doi:10.1152/jn.00042.2003
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Metabotropic Receptor-Mediated Ca2+ Signaling Elevates Mitochondrial Ca2+ and Stimulates Oxidative Metabolism in Hippocampal Slice Cultures

Oliver Kann1, Richard Kovács2 and Uwe Heinemann1

1 Department of Neurophysiology, Charité, Humboldt University, D-10117 Berlin, Germany 2 Department of Neurochemistry, Hungarian Academy of Sciences, Budapest 1025, Hungary

Submitted 15 January 2003; accepted in final form 17 April 2003

Metabotropic receptors modulate numerous cellular processes by intracellular Ca2+ signaling, but less is known about their role in regulating mitochondrial metabolic function within the CNS. In this study, we demonstrate in area CA3 of rat organotypic hippocampal slice cultures that glutamatergic, serotonergic, and muscarinic metabotropic receptor ligands, namely trans-azetidine-2,4-dicarboxylic acid, {alpha}-methyl-5-hydroxytryptamine, and carbachol, transiently increase mitochondrial Ca2+ concentration ([Ca2+]m) as recorded by changes in Rhod-2 fluorescence, stimulate mitochondrial oxidative metabolism as revealed by elevations in NAD(P)H fluorescence, and induce K+ outward currents as monitored by rapid increases in extracellular K+ concentration ([K+]o). Carbachol (1–1,000 µM) elevated NAD(P)H fluorescence by <=14%{Delta}F/F0 and increased [K+]o by <=4.3 mM in a dose-dependent manner. Carbachol-induced responses persisted in Ca2+-free solution and blockade of ionotropic glutamatergic and nicotinic receptors. Under similar conditions caffeine, known to cause Ca2+-induced Ca2+ release (CICR), also evoked elevations in [Ca2+]m, NAD(P)H fluorescence and [K+]o that, in contrast to carbachol-induced responses, displayed oscillations. After depletion of intracellular Ca2+ stores by carbachol in Ca2+-free solution, re-application of 1.6 mM Ca2+-containing solution triggered marked elevations in [Ca2+]m, NAD(P)H fluorescence and [K+]o. These data indicate that metabotropic transmission effectively regulates mitochondrial oxidative metabolism via diverse receptor types in hippocampal cells and that inonitol 1,4,5-trisphosphate-induced Ca2+ release (IICR) or CICR or capacitative Ca2+ entry might suffice in stimulating oxidative metabolism by elevating [Ca2+]m. Thus activation of metabotropic receptors might significantly contribute to generation of ATP within neurons and glial cells.

Address for reprint requests: O. Kann, Abteilung Neurophysiologie, Johannes-Müller-Institut für Physiologie, Universitätsklinikum Charité, Humboldt Universität zu Berlin, Tucholskystrasse 2, D-10117 Berlin, Germany (E-mail: oliver.kann{at}charite.de).




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