ArticleCancer chemotherapy and pharmacology2025
Chronic treatment with carboplatin induces mechanical hypersensitivity and neurochemical changes in the mouse dorsal root ganglia and spinal cord.
Article in Cancer chemotherapy and pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeCarboplatin is a widely used antineoplastic drug, but it is associated with severe adverse effects, including peripheral neuropathy. However, the neurobiological mechanisms underlying this side effect are not fully known. Thus, we determined neurochemical changes in the lumbar dorsal root ganglia (DRG) and spinal cord following carboplatin treatment.
methodsMale BALB/c (23 weeks-old) mice received carboplatin (i.p.; 60 mg/kg/week for 4 weeks) or vehicle. Hindpaw mechanical sensitivity was evaluated at baseline and after carboplatin administration. On day 30 post-first carboplatin administration, mice were euthanized, and the lumbar spinal cord and DRG were processed for immunohistochemistry. Within the L4 DRG, we determined the percentage of neurons expressing the neuropeptide CGRP and the cell injury marker ATF3. Macrophage (CD68, CD163), and blood vessel density (endomucin) were also determined in the DRG. In the spinal cord, we examined the expression of several neuropeptides (CGRP, galanin, NPY) and a marker for astrocyte activation (GFAP).
resultsCarboplatin-treated mice displayed hindpaw mechanical hypersensitivity. The percentage of DRG neurons expressing CGRP and ATF3 as well as the density of CD68⁺ macrophages were significantly greater in carboplatin- compared to vehicle-treated mice. Conversely, the density of CD163
conclusionCarboplatin induced several neurochemical changes in the mouse DRG and spinal cord, which may contribute to the development of carboplatin-induced peripheral neuropathy.
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