Fig. 2
Kcna1 is a downstream target of NMDARs and controls neuronal excitability and dendritic maturation. a Illustrative microdissection of VPM nucleus at P1. VPM nucleus was identified by retrograde labeling from S1 (green labeling). Red arrowheads show the microdissected specimen and its original location. Scale bar: 100 μm. b Top left: Kcna1 expression is decreased in ThGrin1KO (n = 3). Red arrowheads show the labeling in VPM. Student’s t-test, *P < 0.05. Bottom left: in situ hybridization shows decreased Kcna1 expression in ThGrin1KO VPM (n = 3). Scale bar: 200 μm. Right: Kcna1 expression increases during development. c At P15, ThGrin1KO VPM neurons are hyperexcitable; this occludes the effects of the K+ channel blocker BaCl2. (Ctl n = 7, ThGrin1KO n = 4, Ctl + BaCl2 n = 5, ThGrin1KO + BaCl2 n = 5). One-way ANOVA with Tukey's post-hoc test, **P < 0.01, ***P < 0.001, NS, not significant. d At P7, dendritic maturation is impaired by Kcna1 down-regulation (P7 shKcna1 n = 8 from 2 mice). P7 WT and P7 Grin1KOThEpor data reported from Fig. 1b, d. Scale bar: 20 μm. e At P2, dendritic maturation is increased by overexpression of Kcna1 (P2 Kcna1GFP n = 14 from 4 mice). P2 WT and P7 WT data reported from Fig. 1b. Scale bar: 20 μm. WT, wild-type. One-way ANOVA with Tukey's post-hoc test for all statistical tests relating to dendritic complexity, except for Sholl analyses for which a two-way ANOVA with Tukey's post-hoc test was used. *P < 0.05, **P < 0.01, ***P < 0.001; NS, not significant
