The experiments represent the continuation of an ongoing research program aimed at identifying the cellular targets of an injury-induced (sprouted) projection in the mammalian hippocampal formation and to investigate the biological mechanisms(s) which underly this sprouting response. The research plan includes experiments designed to: 1) identify the synaptic targets of sympathohippocampal fibers using electron microscopic techniques, including HRP histochemistry, autoradiography, and degeneration studies 2) test the hypothesis that hippocampal mossy fibers are the source of the putative growth factor released upon septal deafferentation by studying whether sympathetic sprouting will occur in the regio superior of rats, following the lesion-induced growth of mossy fibers into this area, and 3) test the hypothesis that the hippocampal growth activity, which we have recently found to increase in response to medial septal and entorhinal lesions, is related to NGF and is involved in sympathetic and septohippocampal sprouting. There should not be insurmountable technical or theoretical problems which would prevent the acquisition of useful information on the biology of injury-induced neuronal rearrangements and its possible involvement in recovery of function following injury to the CNS.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS017131-08
Application #
3397379
Study Section
Neurology B Subcommittee 1 (NEUB)
Project Start
1987-07-01
Project End
1990-03-31
Budget Start
1988-07-01
Budget End
1990-03-31
Support Year
8
Fiscal Year
1988
Total Cost
Indirect Cost
Name
University of Cincinnati
Department
Type
Schools of Medicine
DUNS #
City
Cincinnati
State
OH
Country
United States
Zip Code
45221
Kudwa, A E; Shoemaker, S E; Crutcher, K A et al. (2002) Evidence for reduced accumulation of exogenous neurotrophin by aged sympathetic neurons. Brain Res 948:24-32
Pettigrew, D B; Levin, L; Crutcher, K A (2000) Sympathetic neurite growth on central nervous system sections is region-specific and unaltered by aging. Neurobiol Aging 21:629-38
Shafer, A J; Crutcher, K A; Isaacson, L G (2000) Remodeling of adult sensory axons in the superior cervical ganglion in response to exogenous nerve growth factor. Brain Res 864:252-62
Kuchel, G A; Crutcher, K A; Naheed, U et al. (1999) NGF expression in the aged rat pineal gland does not correlate with loss of sympathetic axonal branches and varicosities. Neurobiol Aging 20:685-93
Walsh, G S; Krol, K M; Crutcher, K A et al. (1999) Enhanced neurotrophin-induced axon growth in myelinated portions of the CNS in mice lacking the p75 neurotrophin receptor. J Neurosci 19:4155-68
Walsh, G S; Krol, K M; Kawaja, M D (1999) Absence of the p75 neurotrophin receptor alters the pattern of sympathosensory sprouting in the trigeminal ganglia of mice overexpressing nerve growth factor. J Neurosci 19:258-73
Isaacson, L G; Crutcher, K A (1998) Uninjured aged sympathetic neurons sprout in response to exogenous NGF in vivo. Neurobiol Aging 19:333-9
Isaacson, L G; Mareska, M; Nixdorf, W et al. (1997) Dose-dependent response of mature cerebrovascular axons in vivo following intracranial infusion of nerve growth factor. Neurosci Lett 222:21-4
Kawaja, M D; Crutcher, K A (1997) Sympathetic axons invade the brains of mice overexpressing nerve growth factor. J Comp Neurol 383:60-72
Isaacson, L G; Billieu, S C (1996) Increased perivascular norepinephrine following intracerebroventricular infusion of NGF into adult rats. Exp Neurol 139:54-60

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