The excitatory effects of the chemokine CCL2 on DRG somata are greater after an injury of the ganglion than after an injury of the spinal or peripheral nerve.

We compared the expression of chemokine receptor CCR2 protein in the dorsal root ganglia (DRG) injured by the chronic constriction injury (CCI), the spinal nerve ligation (SNL) and a chronic compression of DRG (CCD). Each of these injuries produced the same significant increase in CCR2 protein in the DRG, as assessed by Western blot analyses. Whole-cell patch-clamp recordings revealed that CCL2, a ligand for CCR2 receptor, depolarized nociceptive DRG neurons from rats of the all three models. A greater percentage of these neurons was depolarized by CCL2 after CCD than after either of the other injuries. Furthermore, CCL2 significantly lowered current threshold only in CCD neurons but not in CCI or SNL neurons. CCL2 significantly lowered the net whole-cell potassium currents in neurons after CCD but not after CCI or SNL. Thus, the injury-induced effects of CCL2 in increasing the excitability of the cell bodies of DRG neurons depend on the site of the injury--with greater effects occurring after an injury of the ganglion than after an injury of the spinal or peripheral nerve.