Abstract
In contrast to peripheral nerves, damaged axons in the mammalian brain and spinal cord rarely regenerate. Peripheral nerve injury stimulates neuronal expression of many genes that are not generally induced by CNS lesions, but it is not known which of these genes are required for regeneration. Here we show that co-expressing two major growth cone proteins, GAP-43 and CAP-23, can elicit long axon extension by adult dorsal root ganglion (DRG) neurons in vitro. Moreover, this expression triggers a 60-fold increase in regeneration of DRG axons in adult mice after spinal cord injury in vivo. Replacing key growth cone components, therefore, could be an effective way to stimulate regeneration of CNS axons.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Axons / drug effects
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Axons / metabolism*
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Axotomy
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Calmodulin-Binding Proteins*
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Cell Separation
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / metabolism
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Cytoskeletal Proteins / pharmacology
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GAP-43 Protein / genetics
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GAP-43 Protein / metabolism
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GAP-43 Protein / pharmacology
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Ganglia, Spinal / cytology
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Ganglia, Spinal / drug effects
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Ganglia, Spinal / metabolism
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Gene Expression
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Growth Cones / drug effects
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Growth Cones / metabolism*
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In Vitro Techniques
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Mice
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Mice, Transgenic
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Nerve Growth Factors / biosynthesis
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Nerve Growth Factors / genetics
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Nerve Growth Factors / pharmacology
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Nerve Regeneration / drug effects
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Nerve Regeneration / physiology*
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Nerve Tissue Proteins*
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Neurons / drug effects
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Neurons / metabolism*
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Spinal Cord / cytology
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Spinal Cord / drug effects
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Spinal Cord / metabolism*
Substances
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Basp1 protein, mouse
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Calmodulin-Binding Proteins
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Cytoskeletal Proteins
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GAP-43 Protein
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Nerve Growth Factors
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Nerve Tissue Proteins