Figure 7.

Celsr3 inactivation impairs mGluR1-dependent LTD induction

(A) Left panel, plots of EPSC baseline percentages show mGluR1 agonist DHPG-induced LTP in the control (black) but not in the Celsr3 cKO (red) (P< 0.05, n = 9 PCs from 4 mice in the control; n = 6 PCs from 3 mice in the mutant, Student’s t-test). Right panel: Representative traces of EPSCs before (black) and after (red) LTD induction. The PPR was comparable with and without DHPG perfusion (P> 0.05, n = 5 PCs from 3 mice in each group, Student’s t-test).

(B) In control slices, LTD induction is accompanied by a significant increase of PKCα (red) overexpression in PC dendrites (green, biocytin-labelling) as compared to sham stimulation in the control (left panel). But no PKCα overexpression is observed after PF or sham stimulation in Celsr3 cKO slices (right panel). Quantification in the histogram (∗∗∗, P< 0.001; n = 4 PCs from 3 mice in each group; Student’s t-test).

(C) PCs were immunostained for Calbindin (green) and mGluR1 (red). A significant decrease of mGluR1-postitive particle density in spines is seen in the Celsr3 cKO compared to the control (∗, P< 0.05; Student’s t-test; n = 5).

(D) Western blots of cerebellar samples show decreased mGluR1 protein in the mutant compared to the control.(∗, P< 0.05; Student’s t-test; at least triplicate).