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1
APP deficiency did not affect the mRNA level of <i>Scn8a</i> in cerebellar PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
2
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3
L7 promoter-driven Cre recombinase expression is restricted to PCs in the cerebellar cortex.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
4
Nav1.6 mediated the deficits of PC firing and motor function in APP-null mice.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
5
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6
Exogenous APP expression restored the Nav1.6 currents and ameliorated the abnormalities in the firing patterns of PCs of APP-null mice.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
7
Antibody validation for Nav1.6 and Nav1.1-EGFP in transfected HEK293 cells.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
8
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9
APP deficiency does not alter PC development or induce degeneration.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
10
APP deficiency selectively reduces Nav1.6-mediated Na<sup>+</sup> currents in cerebellar PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
11
Nav1.6 Mediates most of the persistent and resurgent sodium currents in cerebellar PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
12
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13
Exogenous amyloid precursor protein (APP) expression restored the defects of the sIPSCs evoked by Nav1.6-mediated Purkenji cell inputs in APP-null mice.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
14
Cerebellar Purkinje cell (PC)-specific amyloid precursor protein (APP) expression modulates motor function.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
15
PoTX potentiates persistent sodium currents in APP-null PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
16
Validation of Nav1.6 and Nav1.1 contributions to sodium currents in PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
17
Full-length APP is required for the rescue of motor deficit in APP-null mice.
Foilsithe / Cruthaithe 2025Rannpháirtithe: -
18
APP deficiency impairs the normal firing patterns of PCs.
Foilsithe / Cruthaithe 2025Rannpháirtithe: