Titlebook: Sodium Channels, Pain, and Analgesia; Michael J. Parnham (Senior Scientific Advisor),Kev Book 2005 Birkh?user Basel 2005 Nervous System.So

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NaV1.8 as a drug target for pain,ciceptive neurons continues to be regarded as an important contributory event to the onset and/or maintenance of the pain state. As such, molecules that determine nociceptor signalling are prime targets for development of analgesic drugs. Na.1.8 is one of these molecules since (1) its expression is

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Role of voltage-gated sodium channels in oral and craniofacial pain,ars indicates that the biophysical properties, expression pattern and/or distribution of VGSCs are subject to change and that such changes underlie pain associated with injury. The majority of this evidence has come from study of spinal afferents where specific patterns of changes in VGSCs have been

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Future directions in sodium channel research,l excitability in response to external cues. Splice variants, channel editing, post-translational modification and association with accessory proteins all may amplify the repertoire of voltage-gated sodium channels. Using adult inducible knockouts of the various components of sodium channel complexe

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Voltage-gated sodium channels and pain associated with nerve injury and neuropathies,

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Lodewijk V. Dekker,David Cronktrometers was increased by nearly an order of magnitude by the instrument manufacturers. Furthermore, the technique of tandem mass spectrometry (MS/MS) was give978-94-010-5157-6978-94-011-2618-2Series ISSN 1389-2185

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