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J Neurophysiol 90: 3764-3773, 2003. First published August 27, 2003; doi:10.1152/jn.00449.2003
0022-3077/03 $5.00
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Axotomy-Induced Expression of Calcium-Activated Chloride Current in Subpopulations of Mouse Dorsal Root Ganglion Neurons

Sylvain André, Hassan Boukhaddaoui, Brice Campo, Mohammed Al-Jumaily, Véronique Mayeux, Denis Greuet, Jean Valmier and Frédérique Scamps

Institut National de la Santé et de la Recherche Médicale U-583, Université Montpellier II, 34095, Montpellier Cedex 5, France

Submitted 9 May 2003; accepted in final form 10 August 2003

Whole cell patch-clamp recordings of calcium-activated chloride current [ICl(Ca)] were made from adult sensory neurons of naive and axotomized mouse L4–L6 lumbar dorsal root ganglia after 1 day of culture in vitro. A basal ICl(Ca) was specifically expressed in a subset of naive medium-diameter neurons (30–40 µm). Prior nerve injury, induced by sciatic nerve transection 5 days before experiments, increased both ICl(Ca) amplitude and its expression in medium-diameter neurons. Moreover, nerve injury also induced ICl(Ca) expression in a new subpopulation of neurons, the large-diameter neurons (40–50 µm). Small-diameter neurons (inferior to 30 µm) never expressed ICl(Ca). Regulated ICl(Ca) expression was strongly correlated with injury-induced regenerative growth of sensory neurons in vitro and nerve regeneration in vivo. Cell culture on a substrate not permissive for growth, D,L-polyornithine, prevented both elongation growth and ICl(Ca) expression in axotomized neurons. Regenerative growth and the induction of ICl(Ca) expression take place 2 days after injury, peak after 5 days of conditioning in vivo, slowly declining thereafter to control values. The selective expression of ICl(Ca) within medium- and large-diameter neurons conditioned for rapid, efficient growth suggests that these channels play a specific role in postinjury behavior of sensory neuron subpopulations such as neuropathic pain and/or axonal regeneration.

Address for reprint requests and other correspondence: F. Scamps, Inserm U-583, Université Montpellier II, CC089, Place Eugène Bataillon, 34095, Montpellier, Cedex 5, France (E-mail: scamps{at}univ-montp2.fr).




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