A role of
neuropeptides in
neuropathic pain development has been implicated; however, the neuroimmune interactions that are involved in the underlying mechanisms may be more important than previously thought. To examine a potential role of relations between glia cells and
neuropeptides in
neuropathic pain, we performed competitive reverse-transcription polymerase chain reaction (RT-PCR) from the dorsal lumbar spinal cord and the dorsal root ganglion (DRG) after chronic constriction injury (CCI) in the rat sciatic nerve. The RT-PCR results indicated that
complement component 1, q subcomponent (C1q)
mRNA expression was higher than
glial fibrillary acidic protein (GFAP) in the spinal cord 3 and 7 days post-CCI, suggesting that spinal microglia and perivascular macrophages are more activated than astrocytes. In parallel, we observed a strong upregulation of
prodynorphin mRNA in the spinal cord after CCI, with no changes in the expression of
proenkephalin or
pronociceptin. Conversely, the expression of GFAP
mRNA in the DRG was higher than C1q, which suggests that the satellite cells are activated shortly after injury, followed by the macrophages and polymorphonuclear leukocytes infiltrating the DRG. In the DRG, we also observed a very strong upregulation of
prodynorphin (1387%) as well as
pronociceptin (122%) and a downregulation of
proenkephalin (47%) mRNAs. Interestingly, preemptive and repeated i.p. injection of
minocycline reversed the activation of microglia/macrophages in the spinal cord and the trafficking of peripheral immune cells into the DRG, and markedly diminished the upregulation of
prodynorphin and
pronociceptin in the DRG. We thus provide novel findings that inhibition of C1q-positive cells by
minocycline can diminish injury-induced
neuropeptide changes in the DRG. This suggests that immune cells-derived pronociceptive factors may influence
opioid peptide expression. Therefore, the injury-induced activation of microglia and leukocytes and the subsequent activation of
neuropeptides involved in nociception processes are potential targets for the attenuation of
neuropathic pain.