Abstract
Abstract Painful stimuli are detected by specialized neurons, nociceptors, and are translated into action potentials, that are conducted along afferent pathways into the central nervous system, where they are conceived as pain. Voltage-gated sodium channels (NaV channels) are of paramount importance for nociceptor function, as they are responsible for the generation of action potentials and for their directed propagation. The exceptional role of sodium channel subtypes NaV1.7, NaV1.8 and NaV1.9 in the transmission of nociceptive signals has been emphasized by a variety of studies that associated genetically-induced malfunction of these channels with various pain diseases. In the following, structure and function of subtypes NaV1.7, NaV1.8 und NaV1.9 are briefly reviewed, associated pain diseases are introduced and current and future NaV-based strategies for the treatment of pain are discussed.
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