Fig. 4
- ID
- ZDB-FIG-180711-16
- Publication
- McMacken et al., 2018 - The Beta-Adrenergic Agonist Salbutamol Modulates Neuromuscular Junction Formation in Zebrafish Models of Human Myasthenic Syndromes
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Pre-treatment with a selective β2 antagonist blocks the rescue of NMJ development by salbutamol. 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. zMuSK embryos were treated with 5 µm of the selective β2 antagonist ICI118, 551 or control (water) added to E3 medium for 3 h prior to the addition of 20 µm salbutamol. (A) In zebrafish embryos pre-treated with ICI118, 551 no rescue of the axonal pathfinding defects was seen following 21 h of salbutamol treatment, with stalling and branching of motor growth cones (asterisks). (B) Quantification of the effect of pre-treatment of ICI118, 551 on motor axon growth. Following pre-treatment with 5 µm ICI118, 551, salbutamol treatment did not have an effect on axon pathfinding (n.s. P > 0.05, ****P < 0.0001, chi-square test, n = 240 treated and 240 untreated myotomal segments examined). |
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Stage: | Prim-5 |