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Striatal degeneration induced by mitochondrial blockade is prevented by biologically delivered NGF
- Source :
- Journal of Neuroscience Research. 35:452-458
- Publication Year :
- 1993
- Publisher :
- Wiley, 1993.
-
Abstract
- Consistent with the notion that a defect in cellular energy metabolism is a cause of human neurodegenerative disease, systemic treatment with the mitochondrial complex II inhibitor 3-nitropropionic acid (3-NPA) can model the striatal neurodegeneration seen in Huntington's disease. Previously, we have found that nerve growth factor (NGF), delivered biologically by the implantation of a genetically altered fibroblast cell-line, can protect locally against striatal degeneration induced by infusions of high doses of glutamate receptor agonists. We now report that implantation of NGF-secreting fibroblasts reduces the size of adjacent striatal 3-NPA lesions by an average of 64%. We conclude that biologically delivered NGF protects neurons against excitotoxicity and mitochondrial blockade—both energy-depleting processes—implying that appropriate neurotrophic support in the adult brain could protect against neurodegenerative diseases caused in part by energy depletion. © 1993 Wiley-Liss, Inc.
- Subjects :
- Male
medicine.medical_specialty
Tyrosine 3-Monooxygenase
Neurotoxins
Excitotoxicity
medicine.disease_cause
Neuroprotection
Cell Line
Rats, Sprague-Dawley
Cellular and Molecular Neuroscience
Internal medicine
medicine
Animals
Brain Tissue Transplantation
Nerve Growth Factors
Fibroblast
biology
business.industry
Neurodegeneration
Glutamate receptor
Fibroblasts
Nitro Compounds
medicine.disease
Immunohistochemistry
Corpus Striatum
Mitochondria
Rats
Transplantation
Endocrinology
Nerve growth factor
medicine.anatomical_structure
nervous system
Nerve Degeneration
Acetylcholinesterase
biology.protein
Propionates
Energy Metabolism
Genetic Engineering
business
Neurotrophin
Subjects
Details
- ISSN :
- 10974547 and 03604012
- Volume :
- 35
- Database :
- OpenAIRE
- Journal :
- Journal of Neuroscience Research
- Accession number :
- edsair.doi.dedup.....7e327fed75c51c731d41dabff06449ee