Abstract
Animal models of neuropathic pain induce neuronal apoptosis in the spinal cord,1 mediated by caspases. These proteases activate intracellular stress signaling in response to neuroinflammation. Deactivation of the caspase-apoptosis signaling pathway using caspase inhibitors alleviated hypersensitivity.1 Our group demonstrated that multiplexing electrical signals to differentially target glial and neuron cells is more effective than conventional SCS treatments at modulating gene expression in neuroinflammatory processes.
Published Version
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