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1 U 583, INSERM, Montpellier, France
* To whom correspondence should be addressed. E-mail: scamps{at}univ-montp2.fr.
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 one 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 five 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 two days after injury, peak after five 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 post-injury behavior of sensory neuron subpopulations such as neuropathic pain and/or axonal regeneration.
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