Recombinant Rat Sodium channel protein type 1 subunit alpha (Scn1a), partial

1. Nav1.1 in facilitates fast-firing properties in medial septum neurons. Nav1.1 deficits may disrupt information processing in Dravet syndrome via a dysregulation of theta wave brain rhythms. PMID: 26978272
2. Scn1a mutant rats demonstrate a higher hyperthermia-induced seizure susceptibility than wild type rats. PMID: 23375560
3. Hyperthermia-induced seizures occurred in Scn1a mutant rats at high-frequency electroencephalographic oscillations. PMID: 22920678
4. We show that reduction of Nav1.1 expression in the medial septum and diagonal band of Broca leads to a dysregulation of hippocampal oscillations in association with a spatial memory deficit PMID: 23318929
5. In the dorsal horn of the developing rat, Na(v) isoforms are developmentally regulated at the mRNA level in a subtype-specific manner, as Na(v)1.2 and Na(v)1.3 decreased significantly from P3 to adulthood, while Na(v)1.1 was upregulated during this period PMID: 23219908
6. Identification of the cysteine residue responsible for disulfide linkage of Na+ channel alpha and beta2 subunits PMID: 22992729
7. Results suggest that an early increase in dorsal root ganglion Nav1.1 expression after peripheral nerve injury might be involved in the induction of neuropathic pain. PMID: 21714116
8. Hyperthermia-induced seizure-susceptible rats are associated with febrile seizures and display the hyperexcitability of limbic neurons associated with the Scn1a missense mutation. PMID: 20875856
9. An important mechanism of electroacupuncture therapy is its regulation of Nav1.6 and Nav1.1 expression after ischemia. PMID: 20483028
10. Scn1a missense mutation preferentially impairs GABA(A) receptor-mediated synaptic transmission without directly altering the excitability of the pyramidal neurons in the hippocampus, which may be linked to the pathogenesis of febrile seizures. PMID: 20707984
11. TTX-sensitive sodium channel alpha-subunit isoforms Na(v)1.1, Na(v)1.2, Na(v)1.3, Na(v)1.4 and Na(v)1.6 were detected in neonatal rat heart but at levels reduced compared to the predominant cardiac alpha-subunit isoform, Na(v)1.5. PMID: 19426735
12. Quantitative and relative changes in expression of NaCh genes in neurons following injury produced by selective activation of voltage-gated sodium channels. Gene Nav1.1. may play role in neuronal injury/recovery process. PMID: 12835125
13. A novel site of high-density sodium channel clustering in the inner plexiform layer of the retina is described, marked by ankyrin-G and neurofascin. PMID: 15797713
14. these data map the time-dependent loss of Na(v)1.1 mRNA and protein following focal ischemic brain injury PMID: 15878599
15. Na(V)1.1 was distributed in a similar manner to Na(V)1.5: atrial & ventricular myocardium & the left bundle branch, the inferior nodal extension & transitional zone. PMID: 16966585
16. Results suggest that transient cerebral ischemia renders CA1 interneurons less excitable, that depressed excitability involves impaired Na(+) channel activation and that Na(+) channel dysfunction is explained by reduced expression of the Na(v)1.1 subunit. PMID: 17228331
17. This study combined ISH with immunohistochemistry and discovered that most of the PV-immunoreactive cells located at the INL/IPL border express Nav1.1. Our results show that AII amacrine cells express Nav1.1. PMID: 17709186

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KEGG: rno:81574

STRING: 10116.ENSRNOP00000008026

UniGene: Rn.32079