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. 2022 Feb 25;29(9):1744–1756. doi: 10.1038/s41418-022-00959-4

Fig. 2. Deleting Crabp1 causes defects in NMJs.

Fig. 2

A Illustration of lumbrical muscle isolation and subsequent immunostaining experiments and confocal image analyses. B 3D representation of NMJs from WT and CKO lumbrical muscle. White squares 1 and 2 indicate regular-sized NMJs observed in WT mice. White squares 3 and 4 indicate irregular-sized NMJs observed in CKO mice. C NMJ quantification. CKO mice, from 2 to 20 months old, have significantly fewer NMJs as compared to WT mice for each age group (2 months old, n = 8/groups; 9–11 months old, n = 10/groups; 18–20 months old, n = 10/groups). Results are presented as means ± SEM, *p  ≤  0.05, **p  ≤  0.01, compare with WT group. D Immunostaining of NMJs showing axon bundles indicated with axon marker Tuj1 (Red) and acetylcholine receptor (AChR) labeled with αBTX (green). White squares mark axon bundles. Blue arrows indicate the loss AChR clusters at numerous nerve terminals in CKO, especially older (10 months and older), mice. E Enlarged images comparing details of normal and fragmented NMJs. Upper panels, stained with TUJ1 (red), show the morphology of axons and presynaptic terminals. Lower panels show αBTX (green) staining overlaid with TUJ1 staining. White squares mark discontinued AChR (green) clusters and abnormal (fragmented) morphology of NMJ in CKO mice.