Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ

1 II. Physiologisches Institut, Universität Göttingen, D-37073 Göttingen; and 2 Institut für Physiologie, Humboldt-Universität Berlin, Universitätsklinikum Charité, D-10117 Berlin, Germany Schuchmann, S., M. Lückermann, A. Kulik, U. Heinemann, and K. Ballanyi. Ca 2+ - and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ. J. Neurophysiol. 83: 1710-1721, 2000. In hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123) and/or fura-2 via the patch electrode allowed monitoring of mitochondrial potential ( ) changes and intracellular Ca 2+ ([Ca 2+ ] i ) of CA1 pyramidal neurons. Plasmalemmal depolarization to 0 mV caused a mean [Ca 2+ ] i rise of 300 nM and increased Rh-123 fluorescence signal (RFS) by 50% of control. The evoked RFS, indicating depolarization of , and the [Ca 2+ ] i transient were abolished by Ca 2+ -free superfusate or exposure of Ni 2+ /Cd 2+ . Simultaneous measurements of RFS and [Ca 2+ ] i showed that the kinetics of both the Ca 2+ rise and recovery were considerably faster than those of the depolarization. The plasmalemmal Ca 2+ /H + pump blocker eosin-B potentiated the peak of the depolarization-induced RFS and delayed recovery of both the RFS and [Ca 2+ ] i transient. Thus the depolarization due to plasmalemmal depolarization is related to mitochondrial Ca 2+ sequestration secondary to Ca 2+ influx through voltage-gated Ca 2+ channels. CN elevated [Ca 2+ ] i by