Publication Date:
2002-06-08
Description:
The central nervous system (CNS) loses the ability to regenerate early during development, but it is not known why. The retina has long served as a simple model system for study of CNS regeneration. Here we show that amacrine cells signal neonatal rat retinal ganglion cells (RGCs) to undergo a profound and apparently irreversible loss of intrinsic axon growth ability. Concurrently, retinal maturation triggers RGCs to greatly increase their dendritic growth ability. These results suggest that adult CNS neurons fail to regenerate not only because of CNS glial inhibition but also because of a loss of intrinsic axon growth ability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldberg, Jeffrey L -- Klassen, Matthew P -- Hua, Ying -- Barres, Ben A -- 2T32GM07365/GM/NIGMS NIH HHS/ -- R01 EY11030/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1860-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University School of Medicine, Department of Neurobiology, Sherman Fairchild Science Building D231, 299 Campus Drive, Stanford, CA 94305-5125, USA. jlgoldbe@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12052959" target="_blank"〉PubMed〈/a〉
Keywords:
Aging
;
Amacrine Cells/*physiology
;
Animals
;
Animals, Newborn
;
Axons/*physiology/ultrastructure
;
Cell Aging
;
*Cell Communication
;
Cell Separation
;
Cells, Cultured
;
Culture Media, Conditioned
;
Culture Techniques
;
Cyclic AMP/metabolism
;
Dendrites/physiology/ultrastructure
;
Embryo, Mammalian
;
Nerve Regeneration
;
Proto-Oncogene Proteins c-bcl-2/metabolism
;
Rats
;
Retina/cytology
;
Retinal Ganglion Cells/*physiology/transplantation/ultrastructure
;
Signal Transduction
;
Superior Colliculi/physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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