Upregulation of neuregulin-1 reverses signs of neuropathic pain in rats.

摘要: Background: Peripheral nerve injury can result in neuropathic pain, a chronic condition of unclear cause often poorly responsive to current treatments. One possibility is that disrupts large A-fiber-mediated inhibition C-fiber-evoked responses spinal dorsal horn neurons, leading central sensitization. A recent study provided potential molecular mechanism; root ganglion (DRG) neurons secrete neuregulin-1 (NRG1), which binds erbB4 receptors on interneurons and promotes GABA release inhibit nociceptive transmission. Thus, reduced NRG1 expression following could induce pain by disinhibition. We examined if DRG fact rat model exogenous alleviates behavioral signs this condition. Methods: Three models were established rats: spared the tibial common peroneal nerves (SNI model), intraplantar injection complete Freund’s adjuvant (CFA subcutaneous formalin injection. was assessed immunofluorescent staining, hyperalgesia paw withdrawal threshold von Frey filament stimulation, pain-like behavior spontaneous flinching. Results: protein immunoreactivity after SNI. Intrathecal administration neuregulin-1beta 1 (NRG1-1), 62 amino acid mimetic, transiently increased SNI flinching model. Conclusion: Our results are consistent with whereby peripheral reduces NRG1-mediated signaling. Modulating may have therapeutic for treating pain.