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Abstract
Neuropathic pain is mediated by neuroinflammation. We have demonstrated that SCS using differential target multiplexed programming (DTMP) provides significant relief of pain-like behavior in an animal model of neuropathic pain. Transcriptomics and proteomics of the stimulated spinal cord indicates that DTMP regulates biological process involved in neuroinflammation via balancing of perturbed neuron-glial interactions. The mammalian target of rapamycin (mTOR) signaling pathway (directed by protein complexes mTORC1 and mTORC2) has a direct effect on inflammatory pathways. It contains various regulating proteins that can activate or inhibit a pain state. The effect of DTMP and Low-Rate (LR) SCS on mTOR-related proteins will be presented.
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