Action-potential propagation gated by an axonal IA-like K+ conductance in hippocampus

Dominique Debanne (), Nathalie C. Guérineau, Beat H. Gähwiler and Scott M. Thompson
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Dominique Debanne: Unité de Neurocybernétique Cellulaire, UPR9041 CNRS, 280 Bld Sainte Marguerite
Nathalie C. Guérineau: Unité de Neurocybernétique Cellulaire, UPR9041 CNRS, 280 Bld Sainte Marguerite
Beat H. Gähwiler: Brain Research Institute, August Forel-Strasse 1
Scott M. Thompson: Brain Research Institute, August Forel-Strasse 1

Nature, 1997, vol. 389, issue 6648, 286-289

Abstract: Abstract Integration of membrane-potential changes is traditionally reserved for neuronal somatodendritic compartments. Axons are typically considered to transmit reliably the result of this integration, the action potential1, to nerve terminals2,3. By recording from pairs of pyramidal cells in hippocampal slice cultures4,5,6, we show here that the propagation of action potentials to nerve terminals is impaired if presynaptic action potentials are preceded by brief or tonic hyperpolarization. Action-potential propagation fails only when the presynaptic action potential is triggered within the first 15–20 ms of a depolarizing step from hyperpolarized potentials; action-potential propagation failures are blocked when presynaptic cells are impaled with electrodes containing 4-aminopyridine, indicating that a fast-inactivating, A-type K+ conductance is involved. Propagation failed between some, but not all, of the postsynaptic cells contacted by a single presynaptic cell, suggesting that the presynaptic action potentials failed at axonal branch points. We conclude that the physiological activation of an IA-like potassium conductance can locally block propagation of presynaptic action potentials in axons of the central nervous system. Thus axons do not always behave as simple electrical cables: their capacity to transmit action potentials is determined by a time-dependent integration of recent membrane-potential changes.

Date: 1997
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DOI: 10.1038/38502

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