From genes to pain: Na v 1.7 and human pain disorders.
摘要：
Gain-of-function mutations or dysregulated expression of voltage-gated sodium channels can produce neuronal hyperexcitability, leading to acute or chronic pain. The sodium channel Na v1.7 is expressed preferentially in most slowly conducting nociceptive neurons and in sympathetic neurons. Gain-of-function mutations in the Na v1.7 channel lead to DRG neuron hyperexcitability associated with severe pain, whereas loss of the Na v1.7 channel in patients leads to indifference to pain. The contribution of Na v1.7 to acquired and inherited pain states and the absence of motor, cognitive and cardiac deficits in patients lacking this channel make it an attractive target for the treatment of neuropathic pain.
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关键词：
Animals Humans Ganglia, Spinal Neurons Sodium Channels Somatoform Disorders Models, Animal Mutation NAV1.7 Voltage-Gated Sodium Channel
DOI：
10.1016/j.tins.2007.08.004
被引量：
年份：
2007
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