APP deficiency did not affect the mRNA level of <i>Scn8a</i> in cerebellar PCs. ‌ Miao-Jin Ji (22676552)

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Source data and statistical details for figures. ‌ Miao-Jin Ji (22676552)

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L7 promoter-driven Cre recombinase expression is restricted to PCs in the cerebellar cortex. ‌ Miao-Jin Ji (22676552)

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Nav1.6 mediated the deficits of PC firing and motor function in APP-null mice. ‌ Miao-Jin Ji (22676552)

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Raw images for blots. ‌ Miao-Jin Ji (22676552)

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Exogenous APP expression restored the Nav1.6 currents and ameliorated the abnormalities in the firing patterns of PCs of APP-null mice. ‌ Miao-Jin Ji (22676552)

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Antibody validation for Nav1.6 and Nav1.1-EGFP in transfected HEK293 cells. ‌ Miao-Jin Ji (22676552)

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xxx. ‌ Miao-Jin Ji (22676552)

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APP deficiency does not alter PC development or induce degeneration. ‌ Miao-Jin Ji (22676552)

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APP deficiency selectively reduces Nav1.6-mediated Na⁺ currents in cerebellar PCs. ‌ Miao-Jin Ji (22676552)

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Nav1.6 Mediates most of the persistent and resurgent sodium currents in cerebellar PCs. ‌ Miao-Jin Ji (22676552)

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APP-null mice exhibit motor function deficits. ‌ Miao-Jin Ji (22676552)

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Exogenous amyloid precursor protein (APP) expression restored the defects of the sIPSCs evoked by Nav1.6-mediated Purkenji cell inputs in APP-null mice. ‌ Miao-Jin Ji (22676552)

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Cerebellar Purkinje cell (PC)-specific amyloid precursor protein (APP) expression modulates motor function. ‌ Miao-Jin Ji (22676552)

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PoTX potentiates persistent sodium currents in APP-null PCs. ‌ Miao-Jin Ji (22676552)

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Validation of Nav1.6 and Nav1.1 contributions to sodium currents in PCs. ‌ Miao-Jin Ji (22676552)

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Full-length APP is required for the rescue of motor deficit in APP-null mice. ‌ Miao-Jin Ji (22676552)

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APP deficiency impairs the normal firing patterns of PCs. ‌ Miao-Jin Ji (22676552)

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