Deletion of Crmp4 attenuates CSPG-induced inhibition of axonal growth and induces nociceptive recovery after spinal cord injury
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- 作者：Jun Nagaia ; b ; Ryosuke Takayaa ; Wenhui Piaoa ; Yoshio Goshimac ; Toshio Ohshimaa ; ohshima@waseda.jp" class="auth_mail" title="E-mail the corresponding author
- 关键词：5-HT ; 5-hydroxytryptamine ; ANOVA ; analysis of variance ; BMS ; Basso Mouse Scale ; CGRP ; calcitonin gene-related peptide ; CNS ; central nervous system ; CRMP ; collapsin response mediator protein ; ChABC ; chondroitinase ABC ; CSPG ; chondroitin sulfate proteoglycan ; Cdk5 ; cyclin-dependent kinase 5 ; DRG ; dorsal root ganglion ; GFAP ; glial fibrillary acidic protein ; GSK3β ; glycogen synthase kinase 3 beta ; NgR ; nogo receptor ; O/N ; overnight ; PTPσ ; protein tyrosine phosphatase sigma ; RT ; room temperature ; S.E
- 刊名：Molecular and Cellular Neuroscience
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：74
- 期：Complete
- 页码：42-48
- 全文大小：1380 K
文摘
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CRMP4 mediates chondroitin sulfate proteoglycan-induced inhibition of axon growth.
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Enhanced level of CRMP4 in dorsal root ganglion neurons after spinal cord injury
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Crmp4 deletion promotes axonal growth of sensory neurons in injured spinal cord.
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Crmp4 −/− mice showed nociceptive recovery after spinal cord injury.