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. 2020 Apr 20;147(8):dev184069. doi: 10.1242/dev.184069

Fig. 4.

Fig. 4.

Reduced CB1R levels in CFA and growth cones of Klc1−/−. (A) Confocal images of coronal brain sections showing CB1R and L1-NCAM double immunostaining in Klc1+/+ and Klc1−/− mice at P0. (A′,A″) Higher magnification confocal images of boxed areas in panel A showing reduced CB1R levels in CFA at the caudal striatum (A′) and in thalamic regions next to the internal capsule (A″) of Klc1−/− mice (yellow asterisks indicate thalamic region). (B,C) Quantification of CB1R fluorescence intensity normalized to L1-NCAM in in single confocal sections of CFA (B) and thalamus (C). (D) High-resolution spinning disk confocal microscopy image of primary cortical neurons showing CB1R and phalloidin immunostaining in Klc1+/+ and Klc1−/− axonal growth cone (DIV 4). Dashed lines indicate growth cone membrane limit. (E) Quantification of fluorescence intensity of CB1R normalized to phalloidin in growth cones. Data are mean±s.e.m. Klc1+/+, n=4; Klc1−/−, n=5 (B,C) from 3-4 sections; n=60-70 growth cones/genotype from two independent experiments (E). *P<0.01, ****P<0.0001; Student's t-test. cSt, caudal striatum; ic, internal capsule; th, thalamus. Scale bars: 500 μm (A); 100 μm (A′,A″); 20 μm (D).