This article focuses on how mitochondrial activity influences the resilience of nociceptors, or pain-sensing neurons, against excitotoxicity, which is cell death caused by overexcitation and calcium overload. Through a genome-wide screen, the authors identified that the electron transport chain (ETC) is a key determinant of cellular protection. Lowering ETC expression or activity enhances resilience by reducing both oxidative stress (ROS) and the influx of calcium, mitigating cell death in response to excitotoxic agents like capsaicin. Intriguingly, nociceptors naturally maintain a lower expression of ETC components, suggesting an intrinsic mechanism for enduring noxious stimuli compared to other sensory neurons. The study concludes that tuning aerobic respiration serves as a broad protective strategy against various forms of excitotoxic injury.
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