QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, July 8, 2009, 29(27):8649-8654; doi:10.1523/JNEUROSCI.1864-09.2009

This Article Full Text Full Text (PDF) Supplemental Data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Related articles in J. Neurosci. Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Lee, J. K. Articles by Zheng, B. PubMed PubMed Citation Articles by Lee, J. K. Articles by Zheng, B.

 Previous Article  |  Next Article 

Brief Communications
Reassessment of Corticospinal Tract Regeneration in Nogo-Deficient Mice

Jae K. Lee,¹ Andrea F. Chan,¹ Sen M. Luu,¹ Yuhong Zhu,¹ Carole Ho,² Marc Tessier-Lavigne,² and Binhai Zheng¹

¹Department of Neurosciences, University of California San Diego, School of Medicine, La Jolla, California 92093, and ²Division of Research, Genentech Inc., South San Francisco, California 94080

Correspondence should be addressed to Dr. Binhai Zheng, Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, MC 0691, La Jolla, CA 92093-0691. Email: binhai{at}ucsd.edu

The myelin-derived neurite growth inhibitor Nogo has been proposed to play a major role in blocking axon regeneration in the CNS after injuries. However, past studies have produced mixed results regarding the regenerative phenotype of various Nogo-deficient mouse lines after experimental spinal cord injury. Two lines did not display enhanced corticospinal tract (CST) regeneration, and one displayed modest regeneration. A fourth line, a Nogo-A,B gene-trap mutant, was instead reported to exhibit extensive CST regeneration, but the results were later found to be inadvertently confounded with an axon labeling artifact. Of the four Nogo mutant lines studied so far, three continue to express some isoform(s) of Nogo, leaving open the question whether any remaining Nogo protein contributes to the modest regenerative phenotype reported in some. The remaining Nogo mutant line studied was confounded by the unexplained rescue of embryonic lethality associated with this mutation. To gain a better understanding of the contribution of Nogo as an inhibitor of regeneration of CNS axons, and particularly CST axons, we reanalyzed the Nogo-A,B gene-trap mutant line and analyzed a novel, fully viable Nogo deletion mutant line that is null for all known isoforms of Nogo. Our analyses failed to reveal any enhanced CST regeneration after experimental spinal cord injury in either line. These results indicate that Nogo alone does not account for lack of CST regeneration and have implications for current therapeutic development for spinal cord injury in humans by targeting Nogo.

---

Received April 20, 2009; revised May 26, 2009; accepted June 8, 2009.

Correspondence should be addressed to Dr. Binhai Zheng, Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, MC 0691, La Jolla, CA 92093-0691. Email: binhai{at}ucsd.edu

Related articles in J. Neurosci.:

This Week in The Journal

J. Neurosci. 2009 29: i. [Full Text]  

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help