Axonal Na+ Channels Ensure Fast Spike Activation and Back-Propagation in Cerebellar Granule Cells

1 Department of Physiological and Pharmacological Sciences, University of Pavia, Pavia, Italy; 2 Consorzio Nazionale Interuniversitario per le Scienze Fisiche della Materia, Pavia Unit, Pavia, Italy; 3 Department of Mathematics, University of Milan, Milan, Italy; 4 and Department of Biological Scien...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of neurophysiology 2009-02, Vol.101 (2), p.519-532
Hauptverfasser: Diwakar, Shyam, Magistretti, Jacopo, Goldfarb, Mitchell, Naldi, Giovanni, D'Angelo, Egidio
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:1 Department of Physiological and Pharmacological Sciences, University of Pavia, Pavia, Italy; 2 Consorzio Nazionale Interuniversitario per le Scienze Fisiche della Materia, Pavia Unit, Pavia, Italy; 3 Department of Mathematics, University of Milan, Milan, Italy; 4 and Department of Biological Sciences, Hunter College of City University, New York, New York Submitted 20 March 2008; accepted in final form 19 November 2008 In most neurons, Na + channels in the axon are complemented by others localized in the soma and dendrites to ensure spike back-propagation. However, cerebellar granule cells are neurons with simplified architecture in which the dendrites are short and unbranched and a single thin ascending axon travels toward the molecular layer before bifurcating into parallel fibers. Here we show that in cerebellar granule cells, Na + channels are enriched in the axon, especially in the hillock, but almost absent from soma and dendrites. The impact of this channel distribution on neuronal electroresponsiveness was investigated by multi-compartmental modeling. Numerical simulations indicated that granule cells have a compact electrotonic structure allowing excitatory postsynaptic potentials to diffuse with little attenuation from dendrites to axon. The spike arose almost simultaneously along the whole axonal ascending branch and invaded the hillock the activation of which promoted spike back-propagation with marginal delay (
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.90382.2008