Spinal glia activation in oxaliplatin-induced pain

C.A. MIGUEL; M.V. NOYA-RIOBÓ; T. GIOVANNETTI; P.R. BRUMOVSKY; M.J. VILLAR; M.F. CORONEL

Congreso; IASP World Congress on Pain; 2022

International Association for the Study of Pain

Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a frequent and devastating side effect of cancer therapy (1,2). The aim of our work was to evaluate spinal glia activation, glial-neuron communication, and its contribution to oxaliplatin-induced pain. Male young adult rats were injected with oxaliplatin (OXA, 2 mg/kg/day, 3 injections on alternate days, cumulative dose 6 mg/kg, ip) or vehicle (control animals, CTL). Mechanical and thermal allodynia were assessed during 4 weeks by performing von Frey and Choi Tests respectively. The expression of the glial markers GFAP and Iba-1, the pro-inflammatory mediator HMGB1, the cytokines IL1b and TNFa, the neurotrophins NGF and BDNF, the chemokine CXCL12 and its receptor CXCR4, and the neuronal activation marker c-fos, were evaluated in the lumbar spinal cord (SC) 7 days after starting OXA administration by using real time- RT-PCR, immunofluorescence and /or ELISA.Animals receiving OXA developed both mechanical and thermal hypersensitivity and allodynia (p