Skip to main content
Fig. 7 | Skeletal Muscle

Fig. 7

From: NAD+ improves neuromuscular development in a zebrafish model of FKRP-associated dystroglycanopathy

Fig. 7

Supplementation with NAD+ or EmergenC after muscle development does not improve NMJ morphology in fkrp morphants. (A-D4) Anterior left, dorsal top, side-mounted embryos at 72 hpf with labeled AChRs and SV2. (Lettered panels) Merged channels of AChR and SV2. (1) Skeletonized images. (2) Magnification of SV2 channel. (3) Magnification of AChR channel. (4) Magnification of skeleton channel. (A–A4) Control embryo. (B–B4) fkrp morphant embryo exhibiting a reduced degree of distributed innervation within the myotome. (C–C4) fkrp morphant embryo treated with NAD+ at 24 hpf also has reduced innervation. (D–D4) fkrp morphant embryo treated with EmergenC at 24 hpf has reduced NMJs. (E) Length of skeletons per myotome in control embryos (n = 288 half-myotomes), fkrp morphants (n = 303 half-myotomes), and fkrp morphants receiving NAD+ (n = 225 half-myotomes) or EmergenC (n = 225 half-myotomes) at 24 hpf. Note that skeleton length is actually significantly decreased in fkrp morphants receiving NAD+ at 24 hpf. (F) Degree of branching within the myotome in control embryos (n = 283 half-myotomes), fkrp morphants (n = 295 half-myotomes), and fkrp morphants receiving NAD+ (n = 221 half-myotomes) or EmergenC (n = 210 half-myotomes) at 24 hpf. Scalebars are 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ns non-significant

Back to article page