Loss of Whirlin contributes to abnormal paranodal compaction throughout development in the spinal cord. A–J. 2-week, 10, 20, 30, 40-week teased sciatic nerve fibers either wild-type (Aa–Ad, Ca–Cd, Ea–Ed, Ga–Gd, Ia–Id) or Whrn knockout (Ba–Bd, Da–Dd, Fa–Fd, Ha–Hd, Ja–Jd) immunostained against Caspr (Ac–Jc, green), Kv1.2 (Aa–Ja, red), NF186 (Ac–Jc, blue), and merged images (Ad–Jd). Nodal NF186 (Ac–Jc, blue) appear unaffected by age or genotype. In Whrn mutant spinal cords, Caspr (Bb,d; b,d; Fb,d; Hb,d; Jb,d; green) does not compact properly at the paranodes compared to wild-type Caspr (Ab,d; Cb,d; Eb,d; Gb,d; Ib,d; green). In addition, juxtaparanodal marker Kv1.2 (Ba,d; Da,d; Fa,d; Ha,d; Ja,d; red) in Whrn mutant spinal cords shows similar signal intensity and occasional colocalization with Caspr-stained myelin loops. Scale bars (Ad–Jd) = 5 μm. Further quantification and percentages of phenotype-positive spinal cord fibers is included for each age/genotype in a summary graph (bottom).
Green et al. BMC Neuroscience 2013 14:96 doi:10.1186/1471-2202-14-96