Frequency- and spike-timing-dependent mitochondrial Ca signaling regulates the metabolic rate and synaptic efficacy in cortical neurons.

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 Ca 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 Ca responses that were about threefold larger in the somas and apical dendrites than in basal dendrites and axons.

Subcellular Distribution of Persistent Sodium Conductance in Cortical Pyramidal Neurons.

Cortical pyramidal neurons possess a persistent Na current ( ), which, in contrast to the larger transient current, does not undergo rapid inactivation. Although relatively quite small, is active at subthreshold voltages and therefore plays an important role in neuronal input-output processing. The subcellular distribution of channels responsible for and the mechanisms that render them persistent are not known.

Aberrant activity of mitochondrial NCLX is linked to impaired synaptic transmission and is associated with mental retardation.

Calcium dynamics control synaptic transmission. Calcium triggers synaptic vesicle fusion, determines release probability, modulates vesicle recycling, participates in long-term plasticity and regulates cellular metabolism. Mitochondria, the main source of cellular energy, serve as calcium signaling hubs.