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The demonstration of analgesic efficacy of cortistatin in different mouse models is of relevance from a therapeutic point of view, because, in general, there are differences between the pathophysiological mechanisms and responses to drug treatment for neuropathic pain induced by different types of injury to the peripheral nerves [54,55,56]

Critically, these pathways converge on calcium signaling through different mechanisms: GHRH enhances calcium channel activity via PKA phosphorylation, while GHRPs mobilize intracellular calcium stores via IP

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