Unlike most other organs, the brain and other CNS tissues cannot repair itself after injury. The failure of axons to regenerate in these situations is a major cause of sustained neurological deficits after events such as trauma and stroke. This proposal is designed to answer basic questions about why this regeneration fails to occur in order to informatively design therapeutic methods to promote regeneration in vivo. The model system used in this proposal is the retinal ganglion cell (RGC) neuron. RGCs are an excellent tool because they are the only CNS neurons that do not regenerate and can be cultured under conditions in which they will survive but do not regrow axons, allowing axonal regeneration to be specifically addressed. Postnatal (P8) cells re-extend axons in purified cultures at a rate approximately ten times slower than embryonic (E19) cells. This proposal examines why there is a difference in regenerative ability between embryonic and postnatal RGCs, and whether it is a result of intrinsic or extrinsic changes that have occurred in vivo between E19 and P8. In addition to being applicable to other CNS neurons, the use of RGCs allows regeneration in the visual system itself to be specifically elucidated. Glaucoma, optic neuritis, optic nerve ischemia and optic neuropathies all may result in the severing of RGC axons that results in blindness when they fail to regenerate.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32EY007033-03
Application #
6518387
Study Section
Special Emphasis Panel (ZRG1-MDCN-7 (02))
Program Officer
Oberdorfer, Michael
Project Start
2002-04-01
Project End
Budget Start
2002-04-01
Budget End
2003-03-31
Support Year
3
Fiscal Year
2002
Total Cost
$44,212
Indirect Cost
Name
Stanford University
Department
Biology
Type
Schools of Medicine
DUNS #
800771545
City
Stanford
State
CA
Country
United States
Zip Code
94305