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    Scn8a sodium channel, voltage-gated, type VIII, alpha [ Mus musculus (house mouse) ]

    Gene ID: 20273, updated on 2-Oct-2021

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Autistic-like behavior, spontaneous seizures, and increased neuronal excitability in a Scn8a mouse model.

    Autistic-like behavior, spontaneous seizures, and increased neuronal excitability in a Scn8a mouse model.
    Wong JC, Grieco SF, Dutt K, Chen L, Thelin JT, Inglis GAS, Parvin S, Garraway SM, Xu X, Goldin AL, Escayg A.,

    09/18/2021
    Mice Heterozygous for the Sodium Channel Scn8a (Nav1.6) Have Reduced Inflammatory Responses During EAE and Following LPS Challenge.

    Mice Heterozygous for the Sodium Channel Scn8a (Nav1.6) Have Reduced Inflammatory Responses During EAE and Following LPS Challenge.
    Alrashdi B, Dawod B, Tacke S, Kuerten S, Côté PD, Marshall JS., Free PMC Article

    07/3/2021
    Aberrant regulation of a poison exon caused by a non-coding variant in a mouse model of Scn1a-associated epileptic encephalopathy.

    Aberrant regulation of a poison exon caused by a non-coding variant in a mouse model of Scn1a-associated epileptic encephalopathy.
    Voskobiynyk Y, Battu G, Felker SA, Cochran JN, Newton MP, Lambert LJ, Kesterson RA, Myers RM, Cooper GM, Roberson ED, Barsh GS., Free PMC Article

    04/24/2021
    Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Nav 1.6 sodium channels.

    Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Na<sub>v</sub> 1.6 sodium channels.
    Inglis GAS, Wong JC, Butler KM, Thelin JT, Mistretta OC, Wu X, Lin X, English AW, Escayg A.

    02/6/2021
    Sodium channel Nav1.6 in sensory neurons contributes to vincristine-induced allodynia.

    Sodium channel Nav1.6 in sensory neurons contributes to vincristine-induced allodynia.
    Chen L, Huang J, Benson C, Lankford KL, Zhao P, Carrara J, Tan AM, Kocsis JD, Waxman SG, Dib-Hajj SD.

    01/2/2021
    Amyloid beta-Induced Upregulation of Nav1.6 Underlies Neuronal Hyperactivity in Tg2576 Alzheimer's Disease Mouse Model.

    Amyloid β-Induced Upregulation of Na<sub>v</sub>1.6 Underlies Neuronal Hyperactivity in Tg2576 Alzheimer's Disease Mouse Model.
    Ciccone R, Franco C, Piccialli I, Boscia F, Casamassa A, de Rosa V, Cepparulo P, Cataldi M, Annunziato L, Pannaccione A., Free PMC Article

    10/31/2020
    Normal audiogram but poor sensitivity to brief sounds in mice with compromised voltage-gated sodium channels (Scn8a(medJ)).

    Normal audiogram but poor sensitivity to brief sounds in mice with compromised voltage-gated sodium channels (Scn8a<sup>medJ</sup>).
    Heffner RS, Koay G, Heffner HE.

    09/19/2020
    NaV 1.6 regulates excitability of mechanosensitive sensory neurons.

    Na<sub>V</sub> 1.6 regulates excitability of mechanosensitive sensory neurons.
    Israel MR, Tanaka BS, Castro J, Thongyoo P, Robinson SD, Zhao P, Deuis JR, Craik DJ, Durek T, Brierley SM, Waxman SG, Dib-Hajj SD, Vetter I.

    08/15/2020
    Reduction of Scn8a transcript by 25 to 50% delayed seizure onset and lethality in mouse models of SCN8A encephalopathy and Dravet syndrome.

    Scn8a Antisense Oligonucleotide Is Protective in Mouse Models of SCN8A Encephalopathy and Dravet Syndrome.
    Lenk GM, Jafar-Nejad P, Hill SF, Huffman LD, Smolen CE, Wagnon JL, Petit H, Yu W, Ziobro J, Bhatia K, Parent J, Giger RJ, Rigo F, Meisler MH., Free PMC Article

    08/12/2020
    There was a severe and selective decrease of pore-forming voltage-dependent Na(+) channel subunit Nav1.6 in the axon initial segment (AIS) of Purkinje cells. There was a decrease in Nav1.6 protein in the axon intial segment of Purkinje cells, and the consequent tremors in ARF4(+/-)/ARF5(-/-) mice could be alleviated by the PC-specific expression of ARF5 using adeno-ass

    Deletion of Class II ADP-Ribosylation Factors in Mice Causes Tremor by the Nav1.6 Loss in Cerebellar Purkinje Cell Axon Initial Segments.
    Hosoi N, Shibasaki K, Hosono M, Konno A, Shinoda Y, Kiyonari H, Inoue K, Muramatsu SI, Ishizaki Y, Hirai H, Furuichi T, Sadakata T., Free PMC Article

    06/27/2020
    Taken together, our results are consistent with Nav1.6 promoting inflammation and contributing to axonal degeneration following demyelination.

    Nav1.6 promotes inflammation and neuronal degeneration in a mouse model of multiple sclerosis.
    Alrashdi B, Dawod B, Schampel A, Tacke S, Kuerten S, Marshall JS, Côté PD., Free PMC Article

    04/18/2020
    expression level of the NaV1.6 channel, one of the voltage-gated Na(+) channels mainly distributed within the central nervous system, varies in G93A primary motor cortex during ALS disease progression, according to the excitability and INaP alterations, but not in other cortical areas.

    Modified age-dependent expression of NaV1.6 in an ALS model correlates with motor cortex excitability alterations.
    Saba L, Viscomi MT, Martini A, Caioli S, Mercuri NB, Guatteo E, Zona C.

    03/28/2020
    A severe gain-of-function mutation in Scn8a is dependent upon Cre recombinase in an animal model of encephalopathy.

    Prominent role of forebrain excitatory neurons in SCN8A encephalopathy.
    Bunton-Stasyshyn RKA, Wagnon JL, Wengert ER, Barker BS, Faulkner A, Wagley PK, Bhatia K, Jones JM, Maniaci MR, Parent JM, Goodkin HP, Patel MK, Meisler MH., Free PMC Article

    09/21/2019
    we demonstrated that a selective reduction in Scn8a can dramatically protect against the development of spontaneous seizures, hyperactivity, and reactive gliosis in a mouse model of MTLE.

    Selective targeting of Scn8a prevents seizure development in a mouse model of mesial temporal lobe epilepsy.
    Wong JC, Makinson CD, Lamar T, Cheng Q, Wingard JC, Terwilliger EF, Escayg A., Free PMC Article

    11/17/2018
    Rer1 controls the assembly and transport of Nav1.1 and 1.6, the principal sodium channels responsible for recurrent firing, in Purkinje cells.

    The sorting receptor Rer1 controls Purkinje cell function via voltage gated sodium channels.
    Valkova C, Liebmann L, Krämer A, Hübner CA, Kaether C., Free PMC Article

    11/3/2018
    in the absence of Nav1.6 expression, the AIS is occupied by Nav1.2 channels. However, APs are generated in the AIS, and differences in AP propagation to soma and dendrites are minimal.

    Role of sodium channel subtype in action potential generation by neocortical pyramidal neurons.
    Katz E, Stoler O, Scheller A, Khrapunsky Y, Goebbels S, Kirchhoff F, Gutnick MJ, Wolf F, Fleidervish IA., Free PMC Article

    09/22/2018
    Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668.

    Amyloid precursor protein modulates Nav1.6 sodium channel currents through a Go-coupled JNK pathway.
    Li S, Wang X, Ma QH, Yang WL, Zhang XG, Dawe GS, Xiao ZC., Free PMC Article

    06/23/2018
    The results demonstrate that Scn8a plays a vital role in neuronal excitability and provide insight into the mechanism and future treatment of epileptogenesis in early infantile epileptic encephalopathy.

    Neuronal hyperexcitability in a mouse model of <i>SCN8A</i> epileptic encephalopathy.
    Lopez-Santiago LF, Yuan Y, Wagnon JL, Hull JM, Frasier CR, O'Malley HA, Meisler MH, Isom LL., Free PMC Article

    04/14/2018
    Nav1.6 expression at mRNA levels in ischemic and contralateral hemispheres of middle cerebral artery occlusion (MCAO) rats were persistently decreased after reperfusion compared to sham-operated rat, but a prominent, dynamic increase of Nav1.6 immunoreactivity in reactive astrocytes was observed in the genu of corpus callosum in the acute phase. Upregulation of Nav1.6 expression strongly correlated with astrogliosis.

    Transient upregulation of Nav1.6 expression in the genu of corpus callosum following middle cerebral artery occlusion in the rats.
    Zhu H, Lin W, Zhao Y, Wang Z, Lao W, Kuang P, Zhou H.

    02/10/2018
    Differential distribution in primary sensory endings suggests specialized roles for these three NaV isoforms in the process of mechanosensory signaling by muscle spindles.

    Distribution of TTX-sensitive voltage-gated sodium channels in primary sensory endings of mammalian muscle spindles.
    Carrasco DI, Vincent JA, Cope TC., Free PMC Article

    09/23/2017
    that loss of Scn8a leads to altered thalamic reticular nucleus cell intrinsic excitability and a failure in recurrent RT synaptic inhibition

    Regulation of Thalamic and Cortical Network Synchrony by Scn8a.
    Makinson CD, Tanaka BS, Sorokin JM, Wong JC, Christian CA, Goldin AL, Escayg A, Huguenard JR., Free PMC Article

    09/16/2017
    The data of this study support the view that gain-of-function mutations of SCN8A lead to pathogenic alterations in brain function contributing to encephalopathy.

    Altered gene expression profile in a mouse model of SCN8A encephalopathy.
    Sprissler RS, Wagnon JL, Bunton-Stasyshyn RK, Meisler MH, Hammer MF., Free PMC Article

    05/13/2017
    The clinical phenotype of the severe hypomorphic sodium channel gene SCN8A mutant expands the spectrum of Scn8a disease to include a recessively inherited, chronic and progressive movement disorder.

    Single amino acid deletion in transmembrane segment D4S6 of sodium channel Scn8a (Nav1.6) in a mouse mutant with a chronic movement disorder.
    Jones JM, Dionne L, Dell'Orco J, Parent R, Krueger JN, Cheng X, Dib-Hajj SD, Bunton-Stasyshyn RK, Sharkey LM, Dowling JJ, Murphy GG, Shakkottai VG, Shrager P, Meisler MH., Free PMC Article

    12/17/2016
    the presences of Nav1.1, Nav1.6, Navbeta1 and Navbeta3 mRNA and their reduced levels in rat SAN during aging.

    Age-dependent alterations of voltage-gated Na(+) channel isoforms in rat sinoatrial node.
    Huang X, Du Y, Yang P, Lin S, Xi Y, Yang Z, Ma A.

    09/24/2016
    This study demonstrates that Nav channel expression in lumbar motoneurons is altered after SCI, and it shows a tight relationship between the calpain-dependent proteolysis of Nav1.6 channels, the upregulation of I(NaP) and spastici

    Cleavage of Na(+) channels by calpain increases persistent Na(+) current and promotes spasticity after spinal cord injury.
    Brocard C, Plantier V, Boulenguez P, Liabeuf S, Bouhadfane M, Viallat-Lieutaud A, Vinay L, Brocard F.

    08/27/2016
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