|1.||Waxman, Stephen G: 92 articles (09/2015 - 03/2002)|
|2.||Dib-Hajj, Sulayman D: 43 articles (09/2015 - 10/2003)|
|3.||Black, Joel A: 35 articles (09/2015 - 10/2002)|
|4.||George, Alfred L: 28 articles (08/2015 - 01/2002)|
|5.||Wood, John N: 25 articles (01/2015 - 01/2002)|
|6.||Antzelevitch, Charles: 24 articles (01/2014 - 02/2002)|
|7.||Ackerman, Michael J: 22 articles (08/2015 - 08/2002)|
|8.||Cummins, Theodore R: 22 articles (07/2015 - 04/2004)|
|9.||Catterall, William A: 21 articles (08/2015 - 12/2002)|
|10.||Brugada, Ramon: 21 articles (01/2015 - 02/2002)|
01/01/2005 - "The development of sub-type specific blockers has proved slower than anticipated, although the properties of naturally occurring toxin blockers suggest that subtype-specific blockers of sodium channels could be very useful clinically in the treatment of pain."
10/01/2000 - "That blockers of voltage-gated sodium channels (VGSCs) are clinically effective for the treatment of pain associated with certain types of tissue injury suggests that these channels constitute such a target. "
06/01/2000 - "Clinical studies on the efficacy of the sodium channel antagonists in the treatment of acute and chronic pain have had mixed results. "
01/01/2015 - "Human and mouse genetic studies have led to significant advances in our understanding of the role of voltage-gated sodium channels in pain pathways. "
01/01/2015 - "The methods employed in this study can now be applied to future investigations of spinal cord sodium channel plasticity in murine pain models."
|2.||Neuralgia (Stump Neuralgia)
03/01/2011 - "Here we reviewed the roles of sodium channels in neuropathic pain, which may be applicable for the development of new drugs with enhanced efficacy for neuropathic pain treatment."
01/01/2015 - "The present study was conducted to determine changes in the expression of voltage-gated sodium channels (VGSCs) α-subunits after nerve injury and their relation with development of neuropathic pain. "
09/01/2014 - "There has been intense interest in developing inhibitors of the sodium channel Nav1.7 because genetic studies have established very strong validation for the efficacy to alleviate both inflammatory and neuropathic pain. "
11/01/2012 - "In the present study, we investigated whether a novel compound, 2-(2-(4-((4-chlorophenyl)(phenyl)methyl) piperazin-1-yl)-2-oxoethylamino)-N-(3,4,5-trimethoxybenzyl)acetamide (HYP-1), is capable of binding to voltage-gated sodium channels (VGSCs) and evaluated both its inhibitory effect on Na+ currents of the rat dorsal root ganglia (DRG) sensory neuron and its in vivo analgesic activity using rat models of inflammatory and neuropathic pain. "
03/01/2011 - "Recent studies show that in primary sensory neurons, the expression and dynamic regulation of several sodium channel subtypes play important roles in neuropathic pain. "
04/01/2015 - "Our study provides the impetus to investigate whether manipulation of splicing of mammalian voltage-gated sodium channels may be exploitable to provide effective seizure control. "
09/01/2013 - "Future studies should be performed in order to determine whether there are common specific mechanisms of seizure generation related to the sodium channel in these patients. "
03/01/2012 - "Animal studies have revealed new insights into the mechanisms by which mutations in this gene, encoding the type I voltage-gated sodium channel (Na(v)1.1), may lead to seizure activity and cognitive dysfunction. "
07/01/2009 - "In the present study we have examined the correlation between the potency of structurally diverse compounds at voltage-gated sodium channels in vitro and their efficacy in a rodent model of acute generalised seizures induced by electroshock. "
05/01/1985 - "Genetic modifications of voltage-sensitive sodium channels in Drosophila: gene dosage studies of the seizure locus."
08/01/2011 - "Evidence is given for possible advantages related to the higher intrinsic antiepileptic efficacy of BRV and its antiepileptic potential in relation to a wide spectrum of epilepsy forms and for possible disadvantages related to hepatic metabolism and to a lower therapeutic index related to additional intrinsic activity at the sodium channel. "
08/01/2009 - "To evaluate sodium channel genes as candidates for epilepsy susceptibility and their role in therapeutic efficacy, we screened coding single-nucleotide polymorphism of SCN1A p. "
05/01/2014 - "Case-control association study of polymorphisms in the voltage-gated sodium channel genes SCN1A, SCN2A, SCN3A, SCN1B, and SCN2B and epilepsy."
01/01/2007 - "Polymorphisms of drug targets may represent another genetic facet in epilepsy: a recent study demonstrated for the first time a polymorphism of a drug target (the alpha-subunit of a voltage-gated sodium channel) associated in clinical practice with differing response to two classic AEDs. "
11/01/2002 - "Animal experiments, and particularly functional investigations on human chronically epileptic tissue as well as genetic studies in epilepsy patients and their families strongly suggest that some forms of epilepsy may share a pathogenetic mechanism: an alteration of voltage-gated sodium channels. "
04/01/1996 - "A tissue culture bioassay, using the mouse neuroblastoma cell line (Neuro2A), was improved to provide a simple and sensitive bioassay for TTX or sodium channel-blocking toxins (SCB). "
11/01/1983 - "A study was made of the Rb+ transport via activated sodium channels of clone N 18 phi 1 neuroblastoma cells cultured in the Eagle medium with 10% bovine serum. "
02/01/2015 - "The whole-cell patch-clamp technique was used to investigate the effects of eslicarbazepine, CBZ, OXC and LCM on sodium channels endogenously expressed in N1E-115 mouse neuroblastoma cells. "
06/14/2011 - "Apocynum venetum leaf aqueous extract inhibits voltage-gated sodium channels of mouse neuroblastoma N2A cells."
02/01/2009 - "The non-proteolytic BACE1 effect on Nav1.2 current was confirmed in murine neuroblastoma cells, which express sodium channels endogenously, but lack beta2 and beta4. "
|3.||Anticonvulsants (Antiepileptic Drugs)
|7.||Glutamic Acid (Glutamate)
|1.||Deep Brain Stimulation
|2.||Nerve Block (Nerve Blocks)