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The N-methyl-d-aspartate (NMDA) receptor-mediated excitatory procedure, which provides the intracellular Ca2+ increase necessary for nNOS activation, is another mechanism by which UCB-induced neuronal damage occurs

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In this review, we emphasized the latest progress in understanding the mechanisms of IGF in acute and chronic pain, focusing on how IGF affects pain through changes in neuronal excitability, neuroinflammation, and glial cells