Abstract
AbstractThe peripheral nervous system relies upon voltage‐gated sodium channels for encoding and transmitting modality‐specific information into and out of the CNS. These channels are powerful transducers, they signal both pleasant and noxious sensations. They are also considered prime suspects for creating and sustaining the inappropriate excitability in neuronal membranes that is a hallmark of any chronic neuropathic pain syndromes. Curtailing such “pathological hyperexcitability” represents a credible approach to the clinical management of neuropathic pain and this review considers the evidence favoring sodium channels as key players in the injury‐induced hyperexcitability and as targets for pharmacological intervention. Currently used sodium channel therapeutics are discussed together with their limitations and issues. Recent developments in sodium channel biology and pathophysiology are reviewed and ideas for next‐generation sodium channel blocking drugs are considered. Drug Dev. Res. 67:360–375, 2006. © 2006 Wiley‐Liss, Inc.
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