Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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4-Aminopyridine / pharmacology
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Action Potentials / drug effects
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Action Potentials / physiology*
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Animals
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Biological Clocks / physiology
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Dendrites / physiology*
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / physiology*
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In Vitro Techniques
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Models, Neurological
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Neuronal Plasticity / physiology
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Potassium Channel Blockers
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Potassium Channels / metabolism
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Pyramidal Cells / cytology
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiology*
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Rats
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Rats, Wistar
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Reaction Time / physiology
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Sodium Channel Blockers
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Sodium Channels / metabolism
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Somatosensory Cortex / cytology
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Somatosensory Cortex / drug effects
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Somatosensory Cortex / physiology
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Tetrodotoxin / pharmacology
Substances
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Potassium Channel Blockers
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Potassium Channels
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Sodium Channel Blockers
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Sodium Channels
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Tetrodotoxin
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4-Aminopyridine