Spatio-temporal pattern of induction of bradykinin receptors and inflammation in rat dorsal root ganglia after unilateral nerve ligation

Expression of bradykinin receptors was analyzed in freshly isolated dorsal root ganglion neurons of the ipsi- and contralateral segments L4/L5, L2/L3, and T12/T13 two to twenty days after unilateral injury of the adult rat sciatic nerve using gold labeled bradykinin. The number of infiltrating leucocytes was investigated by flow cytometry. Sciatic nerve injury transiently increased the proportion of neurons expressing bradykinin receptors not only in the ipsilateral ganglia L4/L5, but also in the homonymous contralateral ganglia and also bilaterally in the adjacent ganglia L2/L3. Neurons of the ganglia T12/T13 were not affected. The time course of upregulation was different between neurons of the injured nerve and uninjured ones. Furthermore, the proportion of neurons expressing a high density of receptors increased also bilaterally in ganglia L4/L5 and L2/L3. As on the ipsilateral side, the increase in neurons expressing bradykinin receptors in the contralateral homonymous ganglia was due to an induction of the B1 receptor subtype and an upregulation of the B2 subtype. As a possible source for stimulating factors for induction of bradykinin receptors the number of macrophages and lymphocytes was investigated two to twenty days after nerve ligation. No increase was observed prior to day ten and only in ipsilateral ganglia L4/L5, not contralaterally and not in adjacent ganglia L2/L3 and T12/T13. The experiments show that the induction of bradykinin receptors following a unilateral nerve lesion is not restricted to neurons projecting into the damaged nerve but is (i) bilateral, (ii) different in time course between injured and uninjured neurons, and (iii) locally confined to neurons of the adjacent ganglia. Macrophages and lymphocytes are increased after ten day ligation only in the affected ganglia and are probably not involved in the induction of bradykinin receptors. (C) 1999 International Association for the Study of Pain. Published by Elsevier Science B.V.