Amplification of synaptic current by persistent sodium conductance in apical dendrite of neocortical neurons

• Published in: Journal of neurophysiology Vol. 74; no. 5; p. 2220
• Main Authors: Schwindt, P C, Crill, W E
• Format: Journal Article
• Language: English
• Published: United States 01.11.1995
• Subjects: Amplifiers, Electronic; Animals; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Cerebral Cortex - ultrastructure; Dendrites - drug effects; Dendrites - physiology; Electric Conductivity; Iontophoresis; Neurons - drug effects; Neurons - physiology; Neurons - ultrastructure; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Sodium Channels - drug effects; Sodium Channels - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Tetrodotoxin - pharmacology; Time Factors
• ISSN: 0022-3077
• DOI: 10.1152/jn.1995.74.5.2220

1. Evidence for amplification of synaptic current by voltage-gated channels in dendrites of neocortical pyramidal neurons was demonstrated by examining the effect of specific channel blocking agents on the current arriving at the soma during iontophoresis of glutamate at a distal site on the apical dendrite. 2. Dendritic noninactivating Na+ channels were implicated in this voltage-dependent amplification of the transmitted current because it was maintained for > 1 s and because tetrodotoxin (TTX) eliminated much of this amplification. 3. Specific blockers of N-methyl-D-aspartate (NMDA) glutamate receptors reduced the amplitude of the glutamate-evoked current at all potentials and also reduced the non-TTX-sensitive component of voltage-dependent augmentation. The effects of TTX were identical whether or not NMDA channels were blocked. 4. We conclude that a persistent Na+ conductance exists in the apical dendrite of neocortical neurons. Together with the NMDA conductance at the synaptic site it provides a mechanism for the graded, voltage-dependent amplification of tonic, excitatory synaptic input. This amplification results in much more effective transmission of tonic excitatory current to the soma than would occur in a passive dendrite.