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

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, February 21, 2007, 27(8):2124-2134; doi:10.1523/JNEUROSCI.4363-06.2007

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 Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Romero, M. I. Articles by Zhu, Y. Search for Related Content PubMed PubMed Citation Articles by Romero, M. I. Articles by Zhu, Y.

 Previous Article  |  Next Article 

Cellular/Molecular
Deletion of Nf1 in Neurons Induces Increased Axon Collateral Branching after Dorsal Root Injury

Mario I. Romero, ^* Lu Lin, ^* Mark E. Lush, Lei Lei, Luis F. Parada, and Yuan Zhu

Department of Developmental Biology and Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133

Correspondence should be addressed to Dr. Luis F. Parada at the above address. Email: luis.parada{at}utsouthwestern.edu

Ras-mediated signaling pathways participate in multiple aspects of neural development and function. For example, Ras signaling lies downstream of neurotrophic factors and Trk family receptor tyrosine kinases to regulate neuronal survival and morphological differentiation, including axon extension and target innervation. Neurofibromin, the protein encoded by the tumor suppressor gene Nf1, is a negative regulator of Ras [Ras-GAP (GTPase-activating protein)], and we previously demonstrated that Nf1 null embryonic sensory and sympathetic neurons can survive and differentiate independent of neurotrophin support. In this report, we demonstrate that Nf1 loss in adult sensory neurons enhances their intrinsic capacity for neurite outgrowth and collateral branching in vitro and in vivo after dorsal root injury. In contrast to the permanent sensory deficits observed in control mice after dorsal rhizotomy, neuron-specific Nf1 mutant mice spontaneously recover proprioceptive function. This phenomenon appears to be mediated both by a cell-autonomous capacity of spared Nf1–/– DRG neurons for increased axonal sprouting, and by non-cell-autonomous contribution from Nf1–/– neurons in the denervated spinal cord.

Key words: neurofibromin; collateral branching; dorsal rhizotomy; functional recovery; NT-3; regeneration

---

Received May 15, 2006; revised Jan. 2, 2007; accepted Jan. 8, 2007.

Correspondence should be addressed to Dr. Luis F. Parada at the above address. Email: luis.parada{at}utsouthwestern.edu

Related articles in J. Neurosci.:

Mind the GAP: A Role for Neurofibromin in Restricting Axonal Plasticity

Andrew D. Gaudet and Leanne M. Ramer
J. Neurosci. 2007 27: 5533-5534. [Full Text]  

This article has been cited by other articles:

				L. Lin, J. Chen, J. A. Richardson, and L. F. Parada Mice lacking neurofibromin develop gastric hyperplasia Am J Physiol Gastrointest Liver Physiol, October 1, 2009; 297(4): G751 - G761. [Abstract] [Full Text] [PDF]

				A. D. Gaudet and L. M. Ramer Mind the GAP: A Role for Neurofibromin in Restricting Axonal Plasticity J. Neurosci., May 23, 2007; 27(21): 5533 - 5534. [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help