Inhibition of neuropathic pain by decreased expression of the tetrodotoxin-resistant sodium channel, NaV1.8.
作者： Josephine Lai , Michael S. Gold , Chang-Sook Kim , Di Bian , Michael H. Ossipov
DOI: 10.1016/S0304-3959(01)00391-8
关键词: Anesthesia 、 Spinal nerve 、 Neuropathic pain 、 Medicine 、 Sodium channel 、 Peripheral 、 NAV1 、 Pharmacology 、 Sodium channel blocker 、 Dorsal root ganglion 、 Tetrodotoxin
摘要: Neuropathic pain is a debilitating chronic syndrome that often arises from injuries to peripheral nerves. Such has been hypothesized be the result of an aberrant expression and function sodium channels at site injury. Here, we show intrathecal administration specific antisense oligodeoxynucleotides (ODN) tetrodotoxin (TTX)-resistant channel, NaV1.8, resulted in time-dependent uptake ODN by dorsal root ganglion (DRG) neurons, selective "knock-down" reduction slow-inactivating, TTX-resistant current DRG cells. The treatment also reversed neuropathic induced spinal nerve injury, without affecting non-noxious sensation or response acute pain. These data provide direct evidence linking NaV1.8 As restricted sensory this channel offers highly effective molecular target for
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