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Building bridges with astrocytes for spinal cord repair

BioMed Central
Publication Date
DOI: 10.1186/jbiol40
  • Minireview
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Minireview Building bridges with astrocytes for spinal cord repair Robert H Miller Address: Department of Neurosciences, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4975, USA. Email: [email protected] The functional regeneration of neuronal processes in the injured nervous system poses a formidable challenge. During development, axons - the long processes of neurons - grow long distances through complex terrains in stereo- typical patterns to connect with the appropriate targets and facilitate effective communication. Much energy has been expended by researchers in investigating how axonal growth and connectivity are guided and regulated. While a com- plete understanding is still a long way off, it is clear that these are complex processes, involving multiple molecular cues that occur in stereotyped sequences. Many of the cues mediating axonal growth and guidance are lost in the adult central nervous system (CNS) and these processes are further disrupted by injury, resulting in disoriented axons. The injury itself releases inhibitors of axon growth from white matter (bundled tracts of axons) [1,2] and local endogenous glial cells, the supporting non-neuronal cells of the nervous system, respond to the insult with increased production of a variety of growth inhibitors [3,4]. In addition to these environmental changes, there are intrinsic differences in the growth responses of immature and adult axons - adult axons grow less strongly. In consequence, it seems that the key to functional regeneration in the injured adult spinal cord is the simultaneous modification of multiple inhibitory cues - a demanding task that requires a particularly special type of glial cell. In a recent paper in Journal of Biology, Davies et al. [5] describe the identification of such cells and their transplantation to promote a remarkable regeneration of adult axons after spinal cord transection in the rat. The ce

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