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There is an unmet need for efficacious analgesics with lesser adverse effects. Therefore, it is reasonable to consider CGRP + nociceptors as potential analgesic targets. Recently, calcitonin gene-related peptide (CGRP) containing nociceptors were identified as principal coordinators of thermal and mechanical sensitivity in various pain models 7, 8. Peripheral sensitization of dorsal root ganglion (DRG) nociceptors initiates inflammatory pain and is driven by inflammatory mediators released from immune cells and damaged tissue 1, 4, 6. The physiology of inflammatory pain involves the integration of primary afferent neurons, the central nervous system, and the immune system 1, 2, 3, 4, 5. We evidenced sexually dimorphic recovery responses to this pharmacological approach highlighting the importance of sex differences in pain development and response to analgesics. One-time injection of an AP2 inhibitor peptide significantly reduced acute and chronic pain-like behaviors and provided prolonged analgesia.
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We utilized genetic and pharmacological approaches to inhibit nociceptor endocytosis demonstrating its role in the development and maintenance of acute and chronic inflammatory pain. We observed preferential expression of AP2α2, an α-subunit isoform of the AP2 complex, within CGRP +/IB4 - nociceptors in rodents and in CGRP + dorsal root ganglion neurons from a human donor. Here, we identified nociceptor endocytosis as a promising target for local, specific, and long-lasting treatment of inflammatory pain. This therapeutic approach has two inherent pitfalls: specificity and a short duration of action. The advantage of locally applied anesthetics is that they are not associated with the many adverse effects, including addiction liability, of systemically administered analgesics.