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. 2021 Jul 1;24(7):102812. doi: 10.1016/j.isci.2021.102812

Figure 3.

Figure 3

The density of synaptic profiles is decreased in Celsr3 cKO mice

(A and B) Parasagittal cerebellar sections from control (A) and Celsr3 cKO mice (B) stained for Calbindin (red). Overall cerebellar architecture is similar in both genotypes.

(C and D) At higher magnification, Calbindin-positive PC somas and dendritic field are comparable in control (C) and mutant (D) mice. C and D correspond to boxed squares in A and B.

(E and F) Double immunostaining for Calbindin (red) and synaptophysin 38 (SY38, green) in control (E) and mutant (F). SY38-positive dots are abundant in the molecular and the PC layer, and many of them are Calbindin-positive, appearing in yellow.

(G and H) Double immunostaining was for Calbindin (red) and postsynaptic density protein 95 (PSD95, green) in the control (G) and the mutant (H).

(I and J) Decreased densities of SY38-posititive (I) and PSD95-positive (J) profiles in Celsr3 cKO mice compared to control mice. ∗, P< 0.05, Student’s t-test; n = 4 animals in each group. Gross morphology of the cerebellum is comparable in both genotypes groups (arrows).