Assessing the Effects of Paclitaxel Treatment on Glucose Metabolism of Sensory Neurons using Nuclear Magnetic Resonance Spectroscopy

Neuropathic pain arises from damage or disease affecting the somatosensory nervous system, manifesting notably through heightened sensitivity (allodynia) and increased pain response (hyperalgesia). Its prevalence is expected to climb due to factors such as the growing incidence of diabetes mellitus, an aging population, and improved survival rates in cancer patients undergoing chemotherapy. However, a notable drawback of chemotherapy, particularly with agents like Paclitaxel (PTX) used in treating ovarian and breast cancer, is the development of chemotherapy-induced peripheral neuropathy (CIPN), affecting a substantial percentage of patients. PTX, impacting mitochondrial function and elevating reactive oxygen species (ROS) production, exacerbates nociceptor hypersensitivity in the dorsal root ganglion (DRG), a key locus in pain perception post-injury. Inhibition of ROS has shown promise in mitigating anaerobic glycolysis, averting apoptosis, and reducing glucose and lactic acid levels in rat DRG neurons. Elevated levels of these metabolic components in cultured DRG neurons have been linked to diminished cell viability. This study aims to optimize nuclear magnetic resonance protocols for investigating glucose metabolism in the DRG post-PTX administration. The preliminary results will be discussed alongside other supporting data.