Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells.
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.
Goldberg
Jeffrey L
JL
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
MP
Hua
Ying
Y
Barres
Ben A
BA
D000375:Aging; D025042:Amacrine Cells / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D002450:Cell Communication; D002469:Cell Separation; D002478:Cells, Cultured; D016922:Cellular Senescence; D017077:Culture Media, Conditioned; D046508:Culture Techniques; D000242:Cyclic AMP / Q000378:metabolism; D003712:Dendrites / Q000502:physiology / Q000648:ultrastructure; D004622:Embryo, Mammalian; D009416:Nerve Regeneration; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D012160:Retina / Q000166:cytology; D012165:Retinal Ganglion Cells / Q000502:physiology* / Q000637:transplantation / Q000648:ultrastructure; D015398:Signal Transduction; D013477:Superior Colliculi / Q000502:physiology
D017077:Culture Media, Conditioned; D019253:Proto-Oncogene Proteins c-bcl-2; D000242:Cyclic AMP