Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 36, Issue 2, Pages 185-194Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2007.06.011
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Funding
- NIDCR NIH HHS [R01 DE017821] Funding Source: Medline
- NINDS NIH HHS [NS052623, NS038253, R01 NS038253, NS45459, F32 NS045459, R03 NS052623-02, R03 NS052623, R03 NS052623-01] Funding Source: Medline
- PHS HHS [RDE017821A] Funding Source: Medline
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Axonal regeneration within the CNS fails due to the growth inhibitory environment and the limited intrinsic growth capacity of injured neurons. Injury to DRG peripheral axons induces expression of growth associated genes including members of the glial-derived neurotrophic factor (GDNF) signaling pathway and preconditions the injured cells into an active growth state, enhancing growth of their centrally projecting axons. Here, we show that preconditioning DRG neurons prior to culturing increased neurite outgrowth, which was further enhanced by GDNF in a bell-shaped growth response curve. In vivo, GDNF delivered directly to DRG cell bodies facilitated the preconditioning effect, further enhancing axonal regeneration beyond spinal cord lesions. Consistent with the in vitro results, the in vivo effect was seen only at low GDNF concentrations. We conclude that peripheral nerve injury upregulates GDNF signaling pathway components and that exogenous GDNF treatment selectively promotes axonal growth of injury-primed sensory neurons in a concentration-dependent fashion. (c) 2007 Elsevier Inc. All rights reserved.
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