The long-term objective of the proposed research are to understand the neural mechanisms of visual processing, how those mechanisms change, throughout life, and how they are altered to compensate for brain damage. Two specific projects are proposed for the renewal period. The first will continue our investigations of the mechanisms of neural compensation that occurs following visual cortex (VC) damage early in life. Anatomical studies will be carried out in cats to learn more about retinal inputs to the central visual pathways after VC damage, to investigate the nature and mechanisms of enhanced projections that develop from the lateral geniculate nucleus (LGN) to posteromedial lateral suprasylvian (PMLS) cortex following VC damage at different ages, and to determine whether other enhanced projections exist. We also will begin to investigate the biochemical bases of the compensation that occurs following early VC damage. Immunohistochemical studies of the distribution of nerve growth factor (NGF) receptors during normal development and after VC damage will be carried out to learn more about why there is greater potential for compensation in neonates than adults. In addition, we will investigate whether compensation can be increased by administering trophic factors. Together, these experiments will provide information about the mechanisms of recovery from brain damage and possible treatments to improve recovery. The second project will extend our previous work on early visual system development to include changes that occur during aging. Neurophysiological and anatomical studies will be carried out in the retina, LGN, and striate cortex of young adult and old monkeys. The results will be related to changes in human psychophysics during aging, and they will be used to test directly several hypotheses that have been proposed concerning the location and nature of the neural changes that underly vision deficits during aging. These studies will increase our understanding of the relationship between neural structure and function, of the neural mechanisms of declines in visual abilities during aging, and of the affects of aging on the brain in general.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
2R01EY001916-15
Application #
3256318
Study Section
Visual Sciences B Study Section (VISB)
Project Start
1976-06-01
Project End
1995-06-30
Budget Start
1990-07-01
Budget End
1991-06-30
Support Year
15
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
Schools of Arts and Sciences
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
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Spear, P D (1996) Neural plasticity after brain damage. Prog Brain Res 108:391-408
Spear, P D (1996) Afferent and developmentally inherent mechanisms of form and motion processing in cat extrastriate cortex. Prog Brain Res 112:223-30
Kim, C B; Tom, B W; Spear, P D (1996) Effects of aging on the densities, numbers, and sizes of retinal ganglion cells in rhesus monkey. Neurobiol Aging 17:431-8
Danilov, Y; Moore, R J; King, V R et al. (1995) Are neurons in cat posteromedial lateral suprasylvian visual cortex orientation sensitive? Tests with bars and gratings. Vis Neurosci 12:141-51
Spear, P D; Moore, R J; Kim, C B et al. (1994) Effects of aging on the primate visual system: spatial and temporal processing by lateral geniculate neurons in young adult and old rhesus monkeys. J Neurophysiol 72:402-20
Xue, J T; Kim, C B; Moore, R J et al. (1994) Influence of the superior colliculus on responses of lateral geniculate neurons in the cat. Vis Neurosci 11:1059-76

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