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J Neurophysiol (April 30, 2003). doi:10.1152/jn.00042.2003
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Submitted on January 15, 2003
Accepted on April 17, 2003

Metabotropic receptor-mediated Ca2+ signaling elevates mitochondrial Ca2+ and stimulates oxidative metabolism in rat hippocampal slice cultures

Oliver Kann1*, Richard Kovacs2, and Uwe Heinemann1

1 Neurophysiology, Johannes-Mueller-Institute, Charite, Humboldt University, D-10117 Berlin, Germany
2 Neurochemistry, Hungarian Academy of Sciences, Budapest 1025, Hungary

* To whom correspondence should be addressed. E-mail: oliver.kann{at}charite.de.

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 organotypic hippocampal slice cultures that glutamatergic, serotonergic, and muscarinic metabotropic receptor ligands, namely trans-Azetidine-2,4-dicarboxylic acid (ADA), {alpha}-Methyl-5-hydroxytryptamine ({alpha}-Me-5-HT), 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 to 1000 µM) elevated NAD(P)H fluorescence by up to 14 %{Delta}F/F0 and increased [K+]o by up to 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. Following 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 either i) InsP3-induced Ca2+ release (IICR), or ii) CICR, or iii) 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.




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