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J Neurophysiol 101: 1524-1541, 2009. First published December 31, 2008; doi:10.1152/jn.00651.2007
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Quantitative Assessment of the Distributions of Membrane Conductances Involved in Action Potential Backpropagation Along Basal Dendrites

Corey D. Acker and Srdjan D. Antic

Neuroscience Department, University of Connecticut Health Center, Farmington Connecticut

Submitted 12 June 2008; accepted in final form 26 December 2008

Abstract

Basal dendrites of prefrontal cortical neurons receive strong synaptic drive from recurrent excitatory synaptic inputs. Synaptic integration within basal dendrites is therefore likely to play an important role in cortical information processing. Both synaptic integration and synaptic plasticity depend crucially on dendritic membrane excitability and the backpropagation of action potentials. We carried out multisite voltage-sensitive dye imaging of membrane potential transients from thin basal branches of prefrontal cortical pyramidal neurons before and after application of channel blockers. We found that backpropagating action potentials (bAPs) are predominantly controlled by voltage-gated sodium and A-type potassium channels. In contrast, pharmacologically blocking the delayed rectifier potassium, voltage-gated calcium, or Ih conductance had little effect on dendritic AP propagation. Optically recorded bAP waveforms were quantified and multicompartmental modeling was used to link the observed behavior with the underlying biophysical properties. The best-fit model included a nonuniform sodium channel distribution with decreasing conductance with distance from the soma, together with a nonuniform (increasing) A-type potassium conductance. AP amplitudes decline with distance in this model, but to a lesser extent than previously thought. We used this model to explore the mechanisms underlying two sets of published data involving high-frequency trains of APs and the local generation of sodium spikelets. We also explored the conditions under which IA down-regulation would produce branch strength potentiation in the proposed model. Finally, we discuss the hypothesis that a fraction of basal branches may have different membrane properties compared with sister branches in the same dendritic tree.


Address for reprint requests and other correspondence: S. D. Antic, Department of Neuroscience, L4000, UConn Health Center, 263 Farmington Ave., Farmington, CT 06030 (E-mail: antic{at}neuron.uchc.edu)




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Somatic Spikes Regulate Dendritic Signaling in Small Neurons in the Absence of Backpropagating Action Potentials
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[Abstract] [Full Text] [PDF]




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