The Journal of Neuroscience, September 15, 1998, 18(18):7436-7451
Critical Role of Axonal A-Type K+ Channels and Axonal
Geometry in the Gating of Action Potential Propagation along CA3
Pyramidal Cell Axons: A Simulation Study
Irina L.
Kopysova1, 2, 3 and
Dominique
Debanne1
1 Unité de Neurocybernétique Cellulaire,
UPR 9041 Centre National de la Recherche Scientifique, 13009 Marseille, France, 2 Innovationskolleg Theoretische
Biologie, Humboldt-Universität zu Berlin, 10115 Berlin, Germany,
and 3 Unité de Neurobiologie Expérimentale et
Théorie des Systèmes Complexes, UPR 9081 Centre
National de la Recherche Scientifique, 75231 Paris, France
A model of CA3 pyramidal cell axons was used to study a new mode of
gating of action potential (AP) propagation along the axon that depends
on the activation of A-type K+ current
(). The axonal membrane contained voltage-dependent
Na+ channels, K+ channels, and
A-type K+ channels. The density of axonal
A-channels was first determined so that (1) at the resting membrane
potential an AP elicited by a somatic depolarization was propagated
into all axon collaterals and (2) propagation failures occurred when a
brief somatic hyperpolarization preceded the AP induction. Both
conditions were fulfilled only when A-channels were distributed in
clusters but not when they were homogeneously distributed along the
axon. Failure occurs in the proximal part of the axon. Conduction
failure could be determined by a single cluster of A-channels, local
decrease of axon diameter, or axonal elongation. We estimated the
amplitude and temporal parameters of the hyperpolarization required for induction of a conduction block. Transient and small somatic
hyperpolarizations, such as simulated GABAA inhibitory
postsynaptic potentials, were able to block the AP propagation. It was
shown that AP induction had to occur with a short delay (<30 msec)
after the hyperpolarization. We discuss the possible conditions in
which such local variations of the axon geometry and A-channel density
may occur and the incidence of AP propagation failures on hippocampal
network properties.
Key words:
hippocampus; modeling; conduction failure; neural
networks; short-term plasticity; A-current
Copyright © 1998 Society for Neuroscience 0270-6474/98/18187436-16$05.00/0
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