Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathy.

Although it was not statistically significant, we also observed a decreasing trend in spontaneous inhibitory charge transfer in Scn8a D/+ mice (–20,424 ± 4,895 pA × s; P = 0.08; Figure 5E ). sIPSC recordings include both AP-induced synaptic transients as well as mIPSCs, which occur because of spontaneous vesicle fusion in the absence of an AP ( 48 , 49 ).

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I NaR was significantly increased in Scn8a W/+ -PV interneurons (–1,136.0 ± 178.5 pA; P = 0.037), and while we observed an increasing trend, I NaR was not significantly increased in Scn8a D/+ PV interneurons (–952.8 ± 172.9 pA; P = 0.219), when compared to WT (–595.9 ± 84.8 pA) PV interneurons ( Figure 3, G–J ).

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