Zhai, QW (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, 294 Tai Yuan Rd, Shanghai 200031, Peoples R China,firstname.lastname@example.org
Axon degeneration is supposed to be a therapeutic target for treating neurodegenerative diseases. Mauthner cells (M-cells) are ideal for studying axons in vivo because of their limited numbers, large size, and long axons. In this study, we labeled M-cells by single-cell electroporation with plasmids expressing DsRed2 or EGFP. Injury-induced axon degeneration in labeled M-cell was imaged under a confocal microscope, and we found that the Mauthner axons started to degenerate about 24 hr after lesion. The Wld(S) protein containing full-length Nmnat1 is well-known for its axon-protective function in many systems. Overexpression of Wlds in M-cells also greatly delayed axon degeneration in live zebrafish. Nmnat2 is the only Nmnat highly expressed in brain. Here we demonstrated that overexpression of Nmnat2 in M-cells significantly delayed axon degeneration in vivo, and disruption of the NAD synthesis activity of Nmnat2 markedly attenuated its axon-protective function. All these data show that injury-induced axon degeneration of M-cell has a mechanism similar to that in mammalians and would be a valuable model for studying axon degeneration in vivo. (C) 2010 Wiley-Liss, Inc.
Feng, Yan; Yan, Tingting; Zheng, Jin; Ge, Xinjian; Mu, Yu; Zhang, Yi; Wu, Dongmei; Du, Jiu-lin; Zhai, Qiwei.Overexpression of Wld(S) or Nmnat2 in Mauthner Cells by Single-Cell Electroporation Delays Axon Degeneration in Live Zebrafish,JOURNAL OF NEUROSCIENCE RESEARCH,2010,88(15):3319-3327