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Sensory neurones co-express voltage-gated sodium channels that mediate TTX-sensitive (TTX-S) and TTX-resistant (TTX-R) currents, which may contribute to chronic pain after nerve injury. We previously demonstrated that TTX-R channels were decreased acutely in human sensory cell bodies after central axotomy, but accumulated in nerve terminals after peripheral axotomy. We have now studied the TTX-S channels PN1 and Brain III, using specific antibodies for immunohistochemistry, in dorsal root ganglia (DRG) from 10 patients with traumatic central axotomy, nerves from 16 patients with peripheral axotomy, and controls. PN1 showed temporal changes similar to the TTX-R channels in sensory cell bodies of injured DRG. In contrast, Brain III was found only in injured nerves (not control nerves, or control/central axotomy DRG). PNI and Brain III are distinct targets for novel analgesics.


Journal article



Publication Date





495 - 500


Adult, Aged, Antibody Specificity, Brachial Plexus, Cell Line, Female, Ganglia, Spinal, Humans, Kidney, Male, Middle Aged, NAV1.7 Voltage-Gated Sodium Channel, Neuronal Plasticity, Neurons, Afferent, Neuropeptides, Sodium Channels, Tetrodotoxin, Transfection