
We describe a mechanism for coincidence detection mediated by the interaction between backpropagating action potentials and EPSPs in neocortical pyramidal neurons. At distal dendritic locations, appropriately timed EPSPs or oscillations could increase the amplitude of backpropagating action potentials by three- to fourfold. This amplification was greatest when action potentials occurred at the peak of EPSPs or dendritic oscillations and could lead to somatic burst firing. The increase in amplitude required sodium channel activation but not potassium channel inactivation. The temporal characteristics of this amplification are similar to those required for changes in synaptic strength, suggesting that this mechanism may be involved in the induction of synaptic plasticity.
Potassium Channels, 572, dendritic cell, regulatory mechanism, Models, Neurological, Action Potentials, Tetrodotoxin, In Vitro Techniques, Ac, Sodium Channels, excitatory postsynaptic potential, action potential, Biological Clocks, neocortex, Potassium Channel Blockers, Reaction Time, Animals, Keywords: potassium channel, 4-Aminopyridine, Rats, Wistar, Neuronal Plasticity, Pyramidal Cells, article, pyramidal nerve cell, Excitatory Postsynaptic Potentials, nerve cell plasticity, Dendrites, Somatosensory Cortex, oscillation, Rats, priority journal, somatic cell, sodium channel, Sodium Channel Blockers
Potassium Channels, 572, dendritic cell, regulatory mechanism, Models, Neurological, Action Potentials, Tetrodotoxin, In Vitro Techniques, Ac, Sodium Channels, excitatory postsynaptic potential, action potential, Biological Clocks, neocortex, Potassium Channel Blockers, Reaction Time, Animals, Keywords: potassium channel, 4-Aminopyridine, Rats, Wistar, Neuronal Plasticity, Pyramidal Cells, article, pyramidal nerve cell, Excitatory Postsynaptic Potentials, nerve cell plasticity, Dendrites, Somatosensory Cortex, oscillation, Rats, priority journal, somatic cell, sodium channel, Sodium Channel Blockers
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