Fig. 5

The effects of β2 receptor agonist activation on NMJ morphology are replicated by cAMP activation. Lateral views of 24 hpf embryos with neuromuscular synapses labelled with antibodies against SV2 (green, presynaptic vesicles) and αBTX (red, postsynaptic AChRs). Scale bar = 50 µm. (A) zMuSK embryos at 24 hpf demonstrate improvement in AChR clustering and axon pathfinding defects following forskolin treatment. (B) Quantification of motor axon guidance defects. About 88% (n = 28/240) of imaged somites of zMuSK embryos treated with forskolin displayed no axon guidance defects, compared with 41% (n = 142/240) of those in untreated zMuSK embryos. **** indicates P < 0.0001, chi-square test. (C) The number of AChR clusters larger than 20 μm² on myotomal muscle fibres increased with forskolin treatment, with mean number of clusters 0.39 per myotome in untreated embryos, and 1.48 in treated zMuSK embryos. **** indicates P < 0.0001, Student’s t-test, n = 100 treated and 100 untreated myotomes examined.