Some membrane property changes following axotomy in Aδ-type DRG cells are related to cold allodynia in rat

NUMEROUS studies have suggested that changes in electrophysiological properties of primary sensory neurons atter axonal injury contribute to the generation of neuropathic pain. Presently, however, it is unclear which of the changes is important. To address this issue, we performed behavioral and electrophysiological experiments in a double-blind fashion; we made intracellular recordings in the S 1 dorsal root ganglia excised from rats exhibiting cold allodynia behavior after chronic S 1 spinal nerve transaction (allodynia-positive group) and rom rats lacking such behavior after the same nerve injury (allodynia-negative group) or sham injury (sham group). In this study, we sought which of the membrane property changes produced by the spinal nerve injury in each of C-, Aδ- and Aα/β-cell populations was unique to the allodynia-positive group. Analyses of our data revealed that only some changes in Aδ-cells (e.g. the decrease in resting membrane potential and in the threshold of central process) were more pronounced in or unique to the allodynia-positive group. We concluded that certain membrane property changes in the somata and dorsal root axons of Aδ-cells might be important in the generation of cold allodynia.