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Re-establishing the regenerative potential of central nervous system axons in postnatal mice.

Journal article
Authors Kin-Sang Cho
Liu Yang
Bin Lu
Hong Feng Ma
Xizhong Huang
Milos Pekny
Dong Feng Chen
Published in Journal of cell science
Volume 118
Issue Pt 5
Pages 863-72
ISSN 0021-9533
Publication year 2005
Published at Institute of Medical Biochemistry
Pages 863-72
Language en
Keywords Animals, Animals, Newborn, Astrocytes, cytology, metabolism, Axons, metabolism, Blotting, Western, Brain, metabolism, Central Nervous System, physiology, Coculture Techniques, DNA Primers, chemistry, Down-Regulation, Female, Glial Fibrillary Acidic Protein, metabolism, Gliosis, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Models, Anatomic, Nerve Regeneration, Neurons, metabolism, Optic Nerve, anatomy & histology, metabolism, pathology, physiology, Proto-Oncogene Proteins c-bcl-2, metabolism, physiology, Retina, metabolism, Reverse Transcriptase Polymerase Chain Reaction, Transgenes, Vimentin, metabolism
Subject categories Physiology, Cell biology


At a certain point in development, axons in the mammalian central nervous system lose their ability to regenerate after injury. Using the optic nerve model, we show that this growth failure coincides with two developmental events: the loss of Bcl-2 expression by neurons and the maturation of astrocytes. Before postnatal day 4, when astrocytes are immature, overexpression of Bcl-2 alone supported robust and rapid optic nerve regeneration over long distances, leading to innervation of brain targets by day 4 in mice. As astrocytes matured after postnatal day 4, axonal regeneration was inhibited in mice overexpressing Bcl-2. Concurrent induction of Bcl-2 and attenuation of reactive gliosis reversed the failure of CNS axonal re-elongation in postnatal mice and led to rapid axonal regeneration over long distances and reinnervation of the brain targets by a majority of severed optic nerve fibers up to 2 weeks of age. These results suggest that an early postnatal downregulation of Bcl-2 and post-traumatic reactive gliosis are two important elements of axon regenerative failure in the CNS.

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