Dendritic calcium spikes in layer 5 pyramidal neurons amplify and limit transmission of ligand-gated dendritic current to soma.

Long-lasting, dendritic, Ca(2+)-dependent action potentials (plateaus) were investigated in layer 5 pyramidal neurons from rat neocortical slices visualized by infrared-differential interference contrast microscopy to understand the role of dendritic Ca(2+) spikes in the integration of synaptic input. Focal glutamate iontophoresis on visualized dendrites caused soma firing rate to increase linearly with iontophoretic current until dendritic Ca(2+) responses caused a jump in firing rate. Increases in iontophoretic current caused no further increase in somatic firing rate. This limitation of firing rate resulted from the inability of increased glutamate to change evoked plateau amplitude. Similar nonlinear patterns of soma firing were evoked by focal iontophoresis on the distal apical, oblique, and basal dendrites, whereas iontophoresis on the soma and proximal apical dendrite only evoked a linear increase in firing rate as a function of iontophoretic current without plateaus. Plateau amplitude recorded in the soma decreased as the site of iontophoresis was moved farther from the soma, consistent with decremental propagation of the plateau to the soma. Currents arriving at the soma summed if plateaus were evoked on separate dendrites or if subthreshold responses were evoked from sites on the same dendrite. If plateaus were evoked at two sites on the same dendrite, only the proximal plateau was seen at the soma. Just-subthreshold depolarizations at two sites on the same dendrite could sum to evoke a plateau at the proximal site. We conclude that the plateaus prevent current from ligand-gated channels distal to the plateau-generating region from reaching the soma and directly influencing firing rate. The implications of plateau properties for synaptic integration are discussed.