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Glutaminergic mechanisms are involved with opioid-induced hyperalgesia. Reactive astrocytosis prompts neuroglial communication through the presynaptic glutaminergic channels leading to increased threshold responsiveness. The reactive astrocytic phenotype also affects the postsynaptic channel leading to central sensitization. Activated microglia, due to microglial priming, also affect this process. Morphine is depicted as an example opioid, although OIH has been described with almost all opioids (
reproduced with permission from Roekel, Neuroscience, 2016;338:160–82 [26])

Glutaminergic mechanisms are involved with opioid-induced hyperalgesia. Reactive astrocytosis prompts neuroglial communication through the presynaptic glutaminergic channels leading to increased threshold responsiveness. The reactive astrocytic phenotype also affects the postsynaptic channel leading to central sensitization. Activated microglia, due to microglial priming, also affect this process. Morphine is depicted as an example opioid, although OIH has been described with almost all opioids ( reproduced with permission from Roekel, Neuroscience, 2016;338:160–82 [26])

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Purpose of the Review Hyperalgesia may be an iatrogenic consequence of surgery or pain management. Thus, it is essential for anesthesiologists, pain management specialists, surgeons, and primary care physicians to regularly update their awareness and strategies for addressing this problem. This educational review of hyperalgesia provides up-to-date...

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