TY - JOUR
T1 - Assessing Spinal Axon Regeneration and Sprouting in Nogo-, MAG-, and OMgp-Deficient Mice
AU - Lee, Jae K.
AU - Geoffroy, Cédric G.
AU - Chan, Andrea F.
AU - Tolentino, Kristine E.
AU - Crawford, Michael J.
AU - Leal, Marisa A.
AU - Kang, Brian
AU - Zheng, Binhai
N1 - Funding Information:
We thank Marc Tessier-Lavigne, Oswald Steward, and Zhigang He for comments on the manuscript; Sharon Chow, Fang Xie, and Yuhong Zhu for technical assistance. This work was supported by grants from the Roman Reed Research Fund, International Spinal Research Trust, Christopher and Dana Reeve Foundation, the Dana Foundation and NIH/NINDS (R01NS054734). Imaging support was partly provided by the UCSD Neuroscience Microscopy Shared Facility (P30NS047101). J.K.L. is supported by an NRSA Postdoctoral Fellowship (F32NS056697).
PY - 2010/6
Y1 - 2010/6
N2 - A central hypothesis for the limited capacity for adult central nervous system (CNS) axons to regenerate is the presence of myelin-derived axon growth inhibitors, the role of which, however, remains poorly understood. We have conducted a comprehensive genetic analysis of the three major myelin inhibitors, Nogo, MAG, and OMgp, in injury-induced axonal growth, including compensatory sprouting of uninjured axons and regeneration of injured axons. While deleting any one inhibitor in mice enhanced sprouting of corticospinal or raphespinal serotonergic axons, there was neither associated behavioral improvement nor a synergistic effect of deleting all three inhibitors. Furthermore, triple-mutant mice failed to exhibit enhanced regeneration of either axonal tract after spinal cord injury. Our data indicate that while Nogo, MAG, and OMgp may modulate axon sprouting, they do not play a central role in CNS axon regeneration failure.
AB - A central hypothesis for the limited capacity for adult central nervous system (CNS) axons to regenerate is the presence of myelin-derived axon growth inhibitors, the role of which, however, remains poorly understood. We have conducted a comprehensive genetic analysis of the three major myelin inhibitors, Nogo, MAG, and OMgp, in injury-induced axonal growth, including compensatory sprouting of uninjured axons and regeneration of injured axons. While deleting any one inhibitor in mice enhanced sprouting of corticospinal or raphespinal serotonergic axons, there was neither associated behavioral improvement nor a synergistic effect of deleting all three inhibitors. Furthermore, triple-mutant mice failed to exhibit enhanced regeneration of either axonal tract after spinal cord injury. Our data indicate that while Nogo, MAG, and OMgp may modulate axon sprouting, they do not play a central role in CNS axon regeneration failure.
KW - Molneuro
UR - http://www.scopus.com/inward/record.url?scp=77953653088&partnerID=8YFLogxK
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U2 - 10.1016/j.neuron.2010.05.002
DO - 10.1016/j.neuron.2010.05.002
M3 - Article
C2 - 20547125
AN - SCOPUS:77953653088
VL - 66
SP - 663
EP - 670
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 5
ER -