Document Detail

Deletion of Nf1 in neurons induces increased axon collateral branching after dorsal root injury.
MedLine Citation:
PMID:  17314307     Owner:  NLM     Status:  MEDLINE    
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.
Mario I Romero; Lu Lin; Mark E Lush; Lei Lei; Luis F Parada; Yuan Zhu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  27     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-02-22     Completed Date:  2007-03-22     Revised Date:  2007-06-22    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2124-34     Citation Subset:  IM    
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, USA.
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MeSH Terms
Axons / ultrastructure*
Ganglia, Spinal / injuries*,  pathology,  physiopathology*
Gene Deletion*
Gene Silencing
Mice, Knockout
Neurofibromin 1 / deficiency,  genetics*
Neurons, Afferent / metabolism*,  ultrastructure
Recovery of Function
Spinal Cord / metabolism,  physiopathology
Reg. No./Substance:
0/Neurofibromin 1; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases
Comment In:
J Neurosci. 2007 May 23;27(21):5533-4   [PMID:  17522298 ]

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