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

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, July 29, 2009, 29(30):9545-9552; doi:10.1523/JNEUROSCI.1175-09.2009

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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Deng, K. Articles by Filbin, M. T. PubMed PubMed Citation Articles by Deng, K. Articles by Filbin, M. T.

 Previous Article  |  Next Article 

Development/Plasticity/Repair
Increased Synthesis of Spermidine as a Result of Upregulation of Arginase I Promotes Axonal Regeneration in Culture and In Vivo

Kangwen Deng, Huifang He, Jin Qiu, Barbara Lorber, J. Barney Bryson, and Marie T. Filbin

Biology Department, Hunter College, New York, New York 10065

Correspondence should be addressed to Marie T. Filbin, Biology Department, Hunter College, 695 Park Avenue, New York, NY 10065. Email: filbin{at}genectr.hunter.cuny.edu

Adult spinal axons do not spontaneously regenerate after injury. However, if the peripheral branch of dorsal root ganglion neurons is lesioned before lesioning the central branch of the same neurons in the dorsal column, these central axons will regenerate and, if cultured, are not inhibited from extending neurites by myelin-associated inhibitors of regeneration such as myelin-associated glycoprotein (MAG). This effect can be mimicked by elevating cAMP and is transcription dependent. The ability of cAMP to overcome inhibition by MAG in culture involves the upregulation of the enzyme arginase I (Arg I) and subsequent increase in synthesis of polyamines such as putrescine. Now we show that a peripheral lesion also induces an increase in Arg I expression and synthesis of polyamines. We also show that the conditioning lesion effect in overcoming inhibition by MAG is initially dependent on ongoing polyamine synthesis but, with time after lesion, becomes independent of ongoing synthesis. However, if synthesis of polyamines is blocked in vivo the early phase of good growth after a conditioning lesion is completely blocked and the later phase of growth, when ongoing polyamine synthesis is not required during culture, is attenuated. We also show that putrescine must be converted to spermidine both in culture and in vivo to overcome inhibition by MAG and that spermidine can promote optic nerve regeneration in vivo. These results suggest that spermidine could be a useful tool in promoting CNS axon regeneration after injury.

---

Received March 10, 2009; revised June 16, 2009; accepted June 18, 2009.

Correspondence should be addressed to Marie T. Filbin, Biology Department, Hunter College, 695 Park Avenue, New York, NY 10065. Email: filbin{at}genectr.hunter.cuny.edu

Related articles in J. Neurosci.:

This Week in The Journal

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

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help