کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6284991 | 1296732 | 2010 | 6 صفحه PDF | دانلود رایگان |
The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel NaV1.8 is selectively expressed in sensory neurons. It has been reported that NaV1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus NaV1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of NaV1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers.
Research highlightsⶠThe β3 subunit masks the ER retention signal of NaV1.8 and release the channel from the ER. ⶠp11 directly binds to NaV1.8 and help its translocation to the plasma membrane. ⶠPDZD2 is responsible for the functional expression of NaV1.8 on the plasma membrane. ⶠContactin KO mice exhibit a reduction of NaV1.8 along unmyelinated axons in the sciatic nerve. ⶠPKA activation increases the NaV1.8 density on the membrane through direct phosphorylation.
Journal: Neuroscience Letters - Volume 486, Issue 2, 10 December 2010, Pages 78-83