Mitochondrial Dysfunction is Part of a Novel Mechanism for Chemotherapy-Induced Neuropathic Pain

Paclitaxel-induced persistent mechanical allodynia in rats is linked to spinal cord (L1–L6) mitochondrial dysfunction 18 days after the last injection, including reduced oxygen consumption and membrane potential.

• Why it matters: CIPN is common and long-lasting, but how spinal cord mitochondrial impairment sustains pain is unclear, and whether it can be reversed remains unknown.
• What they did: The study measured oxygen consumption, ATP-linked respiration, maximal respiration, electron transfer capacity, and mPTP susceptibility after paclitaxel, tested acute ex-vivo paclitaxel effects, and used cyclosporin A and HBOT; it also delivered healthy mitochondria intrathecally.
• The result: Cyclosporin A reversed paclitaxel-driven mPTP susceptibility, and HBOT improved oxygen consumption and membrane potential while progressively raising mechanical thresholds; intrathecal healthy mitochondria attenuated established allodynia in paclitaxel rats and reduced hypersensitivity in sciatic nerve crush and capsaicin models.

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