Figure 5. Mutant Mice with Disrupted CNS Nodal ECM and Nodal Cytoskeleton.
(A) Loss of ECM molecules in the indicatedmutants at P18. Spinal cord sections were stained as indicated. Scale bar, 5 μm for all panels.
(B) Accelerating rotarod test performed at P18.
(C) Representative images of nodal and paranodal components. P18 optic nerve sections were immunostained as indicated. Note the loss of βIV spectrin in Bcan−/− qv3J double mutants.
(D) Na+ channel staining at nodes of Ranvier (black dots) in the optic nerves of the indicated mutant mice at P18. The density of Na+ channel clusters is reduced in Bcan−/− qv3J double mutants. Scale bars, 20 μm.
(E) Quantitation of the number of Na+ channel clusters per FOV (depicted in D). Data were collected from 20 FOVs from two animals in each group.
(F) P18 spinal cord nodes of Ranvier immunostained using antibodies against Na+ channels (Nav; green) and claudin-11 (red).
(G) Frequency of Na+ channel clusters at nodes. More than 200 nodes (defined by two claudin-11-labeled paranodes) were observed in spinal cords from two animals in each group.
ECM, mutant mice lacking a single ECM molecule; CS, qv3J mice lacking nodal βIV spectrin. *p < 0.01, **p < 0.001; ns, not significant. See also Figure S3 and Movie S2.