Mouse qPCR Primer: Scn8a|NM_011323.3|MQP080235|sodium channel, voltage-gated, type VIII, alpha

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Validated All-in-One™ qPCR Primer for Scn8a(NM_011323.3) [Search again]

Catalog#: MQP080235(click here to view gene annotation page)
Symbol: Scn8a
Species: Mouse
Target Gene Accession: NM_011323.3
Alias: C630029C19Rik, NaCh6, Nav1.6, dmu, med, mnd-2, mnd2, nmf2, nmf335, nmf58, nur14, seal
Gene Description: sodium channel, voltage-gated, type VIII, alpha
Estimated Delivery: 1-3 weeks, but may vary. Please email sales@genecopoeia.com to confirm ETA.

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Important Note: By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.

Gene References into function

med(J) mutation shows greatly reduced levels of Scn8a voltage-gated sodium channels, causing abnormal conduction of action potentials throughout the nervous system and accounting for absence of spontaneous bursting activity in the cochlear nucleus.
Molecular and pathological effects of a modifier gene, Scnm1, on deficiency of the sodium channel Scn8a (Na(v)1.6), in genetic models of movement disorders.
Development of closed-state inactivation was also much faster for Nav1.6 currents than for Nav1.7 currents.
modifier mutation introduces a nonsense codon into SCNM1, a zinc finger protein and putative splice factor; the effect of the modifier mutation is to reduce the abundance of correctly spliced sodium channel transcripts below the threshold for survival
FHF2B, a member of the FGF homologous factor (FHF) subfamily, is an interacting partner of Na(v)1.6.
However, Na(v)1.2 channels show a greater accumulation of inactivation at higher frequencies of stimulation (20-100 Hz) than Na(v)1.6 and thus are likely to generate lower frequencies of firing.
results demonstrate for the first time the intrinsic ability of Na(v)1.6 to produce a resurgent current, and also show that cell background is critical in permitting the generation of these currents
Nav channels generate and regenerate action potentials at multiple sites along the cochlear ganglion cells and nerve fibers, including the afferent endings, ganglionic initial segments, and nodes of Ranvier
Our data supports the hypothesis that the lack of expression of Nav1.6 in Schwann cells at neuromuscular junctions might play a role in the med phenotype.
specialized kinetics of Purkinje Na channels depend directly on Scn8a expression
Beta-scorpion toxin enhance channel activaton, which could make it a model drug to replace deep brain stimulation of the subthalamic nucleus in patients with Parkinson disease.
Inactivation of sodium channel Scn8A (Na-sub(v)1.6) in Purkinje neurons impairs learning in Morris water maze and delay but not trace eyeblink classical conditioning.
Both Na(v)1.2 and Na(v)1.1 channels accumulated at initial segments and nodes of med GCs, sites normally occupied by Na(v)1.6 in mice lacking Na(v)1.6
Hyperpolarizations that approximated synaptic inhibition effectively recovered channels, suggesting that increases in Na channel availability promote rebound firing after inhibition.
an electrically induced signal can propagate along the vessel axis via the endothelium and can induce sequential activation of Na(v) and Ca(v)3.2 channels.
4,9-anhydro-tetrodotoxin selectively blocks Scn8a sodium channel.
The data showed that subthreshold sodium currents are critical determinants of Mes V electrogenesis and burst generation and suggest a role for resurgent sodium currents in control of spike discharge.
mutants were more seizure resistant than wild-type littermates, suggesting that altered Na(v)1.6 function reduces neuronal excitability
Results suggest that GABAA receptors in the medial vestibular nucleus are up-regulated in mice with greatly reduced expression of Scn8a sodium channels. There was no significant effect on GABAB receptors.
Nav1.6 channels in globus pallidus neurons are distinguished from those found in many regular spiking neurons by a prominent resurgent gating mode.
Together, these data suggest that Scn8a plays a critical role in emotional behavior in mice.
The unique properties of Na(V)1.6 channels, together with the resurgent currents that they conduct in neurons, make these channels well-suited to provide the driving force for sustained repetitive firing, a crucial property of neurons.
Na(v)1.6 channels normally occupy most of the molecular machinery responsible for channel clustering because they have higher binding affinity
NaV1.6 subunits at the axon initial segment contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons
Multiple receptor-dependent mechanisms operating at all stages of B cell development limit the contribution of B cells with Dmu heavy chain alleles to the repertoire.