Research Topics
| Mark EstacionSummaryAffiliation: Yale University Country: USA Publications
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Publications
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neuronsMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Exp Neurol 224:362-8. 2010..Our data provide a pathophysiological basis for the pathogenicity of the first epilepsy-linked mutation within Na(V)1.3 channels and hippocampal neurons...- A sodium channel gene SCN9A polymorphism that increases nociceptor excitabilityMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven CT
Ann Neurol 66:862-6. 2009..Our results suggest that polymorphisms in the Na(V)1.7 channel may influence susceptibility to pain... 
Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitableSulayman D Dib-Hajj
Deptartment of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Mol Pain 4:37. 2008..Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective...- Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channelYang Yang
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
Nat Commun 3:1186. 2012..We suggest that this approach might identify variants that confer enhanced pharmacoresponsiveness on a variety of channels... - Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7Mark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Mol Pain 7:92. 2011..In this paper we describe three patients who house the NaV1.7/I228M variant... - A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgiaTanya Z Fischer
Department of Neurology, Yale University School of Medicine, New Haven, CT 16510, USA
Ann Neurol 65:733-41. 2009..Inherited erythromelalgia (IEM) has been linked to gain-of-function mutations of Na(v)1.7. We now report a novel mutation (V400M) in a three-generation Canadian family in which pain is relieved by carbamazepine (CBZ)... - A new Nav1.7 mutation in an erythromelalgia patientMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Biochem Biophys Res Commun 432:99-104. 2013..9 mV), which is predicted to attenuate the effect of this mutation on DRG neuron firing. These changes are consistent with previously characterized Erytheromelalgia associated mutations of Nav1.7... - Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitabilityMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Mol Pain 6:35. 2010..7 and on DRG neuron excitability have not been investigated. We used voltage- and current-clamp recordings to evaluate the hypothesis that ranolazine may be effective in regulating Nav1.7-induced DRG neuron hyperexcitability... - The response of Na(V)1.3 sodium channels to ramp stimuli: multiple components and mechanismsMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
J Neurophysiol 109:306-14. 2013.... - Nav1.9, G-proteins, and nociceptorsStephen G Waxman
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
J Physiol 586:917-8. 2008