Fig. 1.

Gprasp2 knockout mice display structural alterations in hippocampal neurons. a Gprasp2 deletion targeting strategy. b In situ hybridization for Gprasp2 mRNA detects strong signal in P15 WT mice and no signal in Gprasp2^−/y mice. Scale bar, 1 mm. c Western blotting shows the deletion of GPRASP2 in whole-brain lysates from KO mice. d Expression pattern of GPRASP2 in brain lysates of WT mice from E18 to 3-month of age; n = 3 mice. e–g Coronal section from P15 WT mice reveals Gprasp2 is highly expressed in (f) the hypothalamus and in (g) the hippocampal formation. Scale bar, 2 mm in (e) and 250 µm in (f–g). h Representative images from the CA1 region in AAV9.hSyn.GFP infected mice. High-magnification images of Gprasp2^−/y and WT CA1 pyramidal neurons. Scale bar, 100 µm. i Sholl analysis reveals decreased neuronal complexity of Gprasp2^−/y CA1 pyramidal neurons compared with WT littermates; WT n = 22/3 neurons/mice, KO n = 22/3 neurons/mice; two-way repeated measures ANOVA. Inset (top), representative CA1 neurons. Inset (bottom), total dendritic length in distal (260–500 µm) but not proximal (0–240 µm) regions is reduced in Gprasp2^−/y; one-way ANOVA with Bonferroni post hoc. All data are presented as mean ± s.e.m. Statistical significance: *p < 0.05, **p < 0.01