Home LiteratureArticle Details
PMID: 12052959 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells.

Science (New York, N.Y.) ·Vol. 296 ·No. 5574 ·2002-06-07 ·Pages 1860-4

Goldberg JL, Klassen MP, Hua Y, Barres BA

Abstract

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.

MeSH Terms
Aging Amacrine Cells/physiology Animals Animals, Newborn Axons/physiology,ultrastructure Cell Communication Cell Separation Cells, Cultured Cellular Senescence 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
Chemicals
Culture Media, Conditioned Proto-Oncogene Proteins c-bcl-2 Cyclic AMP
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Goldberg Jeffrey L
Stanford University School of Medicine, Department of Neurobiology, Sherman Fairchild Science Building D231, 299 Campus Drive, Stanford, CA 94305-5125, USA. jlgoldbe@stanford.edu
Klassen Matthew P
Hua Ying
Barres Ben A
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
1095-9203
Published
2002-06-07
Pages
1860-4
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NIGMS NIH HHS · 2T32GM07365 · United States
NEI NIH HHS · R01 EY11030 · United States
Corrections
CommentIn
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