Fig. 3
Surfen and oxalyl surfen rescue motoneuron defects and functional deficits in Tg[HuC::hTauP301L; DsRed] embryos. a Immunohistochemical visualization of the synaptotagmin II protein (anti-znpl antibody) in 72 hpf wild-type (WT) and Tg[HuC::hTauP301L; DsRed] (hTauP301L) embryos treated for 2 days with 1% DMSO (hTauP301L + 1% DMSO), 80 mM LiCl (hTauP301L + LiCl), 3 μM surfen (hTauP301L + surfen), 2 μM oxalyl surfen (hTauP301L + oxalyl surfen) or 3 μM hemisurfen (hTauP301L + hemisurfen), showed that surfen and oxalyl surfen markedly rescued the motorneuron axon defects seen in Tg[HuC::hTauP301L; DsRed] embryos. The imaged caudal area corresponds to the box represented in (b). Scale bar: 50 μm. c Quantification of the mean axonal branch number in the framed caudal area (b) of Tg[HuC::hTauP301L; DsRed] embryos treated as in (a). The number of axonal branches was significantly increased in Tg[HuC::hTauP301L; DsRed] embryos treated with surfen and oxalyl surfen when compared with their age-matched 1% DMSO siblings (n = 10, ***P < 0.001; **P < 0.01; *P < 0.05; ns: non-significant, Student’s t test). d Quantification of fluorescence staining intensity of znp1 labeling in the framed caudal area (b) of Tg[HuC::hTauP301L; DsRed] embryos treated as in (a). Results showed that the fluorescence intensity of the znp1 staining was significantly increased in Tg[HuC::hTauP301L; DsRed] embryos following surfen and oxalyl surfen treatments when compared with their age-matched 1% DMSO siblings (n = 10, **P < 0.01; *P < 0.05, ns: non-significant, Student’s t test). e The touch evoked escape response was used to probe the motor behavior of Tg[HuC::hTauP301L; DsRed] embryos treated for 1 day with 80 mM LiCl, 3 μM surfen, 2 μM oxalyl surfen or 3 μM hemisurfen. The motor defect observed in Tg[HuC::hTauP301L; DsRed] embryos was significantly rescued following treatment with surfen and oxalyl surfen, but not hemisurfen (n = 250, *P < 0.05, ns: non-significant, Student’s t test)