Neuropathic pain develops normally in mice lacking both Nav1.7 and Nav1.8

Two voltage gated sodium channel alpha-subunits, Na(v)1.7 and Na(v)1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain. Misexpression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Na(v)1.7 and Na(v)1.8 is uncertain. Here we show that deleting Na(v)1.7 has no effect on the development of neuropathic pain. Double knockouts of both Na(v)1.7 and Na(v)1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds. These studies demonstrate that, in contrast to the highly significant role for Na(v)1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Na(v)1.7 or Na(v)1.8 alone or in combination.