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J Neurophysiol 94: 4145-4155, 2005; doi:10.1152/jn.00521.2005
0022-3077/05 $8.00
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Signal Propagation in Oblique Dendrites of CA1 Pyramidal Cells

Michele Migliore1,2, Michele Ferrante3 and Giorgio A. Ascoli3,4

1Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut; 2Institute of Biophysics, National Research Council, Palermo, Italy; 3Krasnow Institute for Advanced Study and 4Psychology Department, George Mason University, Fairfax, Virginia

Submitted 19 May 2005; accepted in final form 17 August 2005

The electrophysiological properties of the oblique branches of CA1 pyramidal neurons are largely unknown and very difficult to investigate experimentally. These relatively thin dendrites make up the majority of the apical tree surface area and constitute the main target of Schaffer collateral axons from CA3. Their electrogenic properties might have an important role in defining the computational functions of CA1 neurons. It is thus important to determine if and to what extent the back- and forward propagation of action potentials (AP) in these dendrites could be modulated by local properties such as morphology or active conductances. In the first detailed study of signal propagation in the full extent of CA1 oblique dendrites, we used 27 reconstructed three-dimensional morphologies and different distributions of the A-type K+ conductance (KA), to investigate their electrophysiological properties by computational modeling. We found that the local KA distribution had a major role in modulating action potential back propagation, whereas the forward propagation of dendritic spikes originating in the obliques was mainly affected by local morphological properties. In both cases, signal processing in any given oblique was effectively independent of the rest of the neuron and, by and large, of the distance from the soma. Moreover, the density of KA in oblique dendrites affected spike conduction in the main shaft. Thus the anatomical variability of CA1 pyramidal cells and their local distribution of voltage-gated channels may suit a powerful functional compartmentalization of the apical tree.


Address for reprint requests and other correspondence: M. Migliore, Dept. of Neurobiology, Yale University School of Medicine, New Haven, CT06520 (E-mail: michele.migliore{at}yale.edu)




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