Partial sciatic nerve ligation induces increase in the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) in astrocytes in the lumbar spinal dorsal horn and the gracile nucleus.

The activation of glial cells in the spinal dorsal horn and the gracile nucleus by inflammation and nerve injury has been suggested to be involved in neuronal plasticity and central sensitization, hence contributing to tactile allodynia. The aim of this study was to determine the possible intracellular signal transduction pathway associated with glial cells, which have been activated by partial sciatic nerve ligation (PSNL), a well-characterized rat model of neuropathic pain. At 3 weeks post-lesion, PSNL markedly increased glia fibrillary acidic protein (GFAP) immunoreactive (IR) astrocytes in both the L4-5 spinal dorsal horn and the gracile nucleus. Moreover, PSNL increased the phosphorylation of mitogen activated protein (MAP) kinases, including the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), but not p38, in glia-like cells in these same areas. Both phosphorylated (p) ERK- and JNK-IR cells were co-localized with GFAP, suggesting their expression in reactive astrocytes. In summary, our data indicate that PSNL activates ERK/MAP and JNK/MAP kinase pathways in astrocytes in the dorsal horn and the gracile nucleus, these events possibly being involved in the pathogenesis of neuropathic pain. Copyright 2002 International Association for the Study of Pain