Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Yana Khrapunsky
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Israel Melamed
Department of Neurosurgery, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Grace Stutzmann
Rosalind Franklin University of Medicine and Science, Chicago Medical School, Center for Neurodegenerative Disease and Therapeutics, North Chicago, United States
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Israel Sekler
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben–Gurion University of the Negev, Beer Sheva, Israel
Mitochondrial activity is crucial for the plasticity of central synapses, but how the firing pattern of pre- and postsynaptic neurons affects the mitochondria remains elusive. We recorded changes in the fluorescence of cytosolic and mitochondrial Ca2+ indicators in cell bodies, axons, and dendrites of cortical pyramidal neurons in mouse brain slices while evoking pre- and postsynaptic spikes. Postsynaptic spike firing elicited fast mitochondrial Ca2+ responses that were about threefold larger in the somas and apical dendrites than in basal dendrites and axons. The amplitude of these responses and metabolic activity were extremely sensitive to the firing frequency. Furthermore, while an EPSP alone caused no detectable Ca2+ elevation in the dendritic mitochondria, the coincidence of EPSP with a backpropagating spike produced prominent, highly localized mitochondrial Ca2+ hotspots. Our results indicate that mitochondria decode the spike firing frequency and the Hebbian temporal coincidences into the Ca2+ signals, which are further translated into the metabolic output and most probably lead to long-term changes in synaptic efficacy.
