S
Stephen G. Waxman
Researcher at Yale University
Publications - 866
Citations - 64432
Stephen G. Waxman is an academic researcher from Yale University. The author has contributed to research in topics: Sodium channel & Dorsal root ganglion. The author has an hindex of 130, co-authored 836 publications receiving 60119 citations. Previous affiliations of Stephen G. Waxman include Veterans Health Administration & United States Department of Veterans Affairs.
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Journal ArticleDOI
International Union of Pharmacology. XLVIII. Nomenclature and Structure-Function Relationships of Voltage-Gated Calcium Channels
TL;DR: The molecular relationships and physiological functions of these calcium channel proteins are presented and comprehensive information on their molecular, genetic, physiological, and pharmacological properties is provided.
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Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger
TL;DR: The results suggest that differences in the pathophysiology of gray and white matter anoxic injury are likely to necessitate multiple strategies for optimal CNS protection, and suggest that Ca2+ loading might occur via reverse operation of the Na(+)-Ca2+ exchanger.
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Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury
Bryan C. Hains,Stephen G. Waxman +1 more
TL;DR: An important role for activated microglia in the maintenance of chronic central below-level pain after SCI is suggested and the newly emerging role of non-neuronal immune cells as a contributing factor in post-SCI pain is supported.
Journal ArticleDOI
Determinants of conduction velocity in myelinated nerve fibers.
TL;DR: The conduction speed of any given fiber reflects a number of parameters and is not determined by any single structural characteristic.
Journal ArticleDOI
Sodium Channels in Normal and Pathological Pain
TL;DR: The contribution of voltage-gated sodium channels to pain is reviewed, with Na(v)1.7 is of special interest because it has been linked to a spectrum of inherited human pain disorders and is upregulated along pain-signaling pathways after nervous system injuries.