Expression of the growth-associated protein GAP-43 in adult rat retinal ganglion cells following axon injury.
We have studied the expression of the growth-associated protein GAP-43 after injury to the axons of adult rat retinal ganglion cells (CNS neurons that do not normally regenerate injured axons). Both the biosynthetic labeling of GAP-43 and the GAP-43 immunoreactivity of the retina increased after axotomy, but only when the injury was within 3 mm of the eye. These results suggest the following conclusions: First, axon injury is sufficient to alter GAP-43 expression in CNS neurons, even in the absence of regeneration. Second, mechanisms that regulate GAP-43 expression are sensitive to the length of uninterrupted axon remaining after injury. Finally, the conditions that favor increased GAP-43 are similar to those that favor regrowth of injured CNS axons into grafts of peripheral nerve, suggesting that GAP-43 induction is accompanied by an increased potential of injured CNS neurons to regenerate.
Doster
S K
SK
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110.
Lozano
A M
AM
Aguayo
A J
AJ
Willard
M B
MB
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000502:physiology*; D001692:Biological Transport; D019922:GAP-43 Protein; D006133:Growth Substances / Q000378:metabolism; D006652:Histological Techniques; D007158:Immunologic Techniques; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D051381:Rats; D012165:Retinal Ganglion Cells / Q000378:metabolism*
D019922:GAP-43 Protein; D006133:Growth Substances; D008562:Membrane Glycoproteins; D009419:Nerve Tissue Proteins