Striatal degeneration induced by mitochondrial blockade is prevented by biologically delivered NGF

J Neurosci Res. 1993 Jul 1;35(4):452-8. doi: 10.1002/jnr.490350413.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylcholinesterase / metabolism
  • Animals
  • Brain Tissue Transplantation / physiology
  • Cell Line
  • Corpus Striatum / anatomy & histology
  • Corpus Striatum / drug effects*
  • Corpus Striatum / ultrastructure
  • Energy Metabolism / physiology
  • Fibroblasts / metabolism
  • Genetic Engineering
  • Immunohistochemistry
  • Male
  • Mitochondria / drug effects*
  • Nerve Degeneration / drug effects*
  • Nerve Growth Factors / genetics
  • Nerve Growth Factors / metabolism
  • Nerve Growth Factors / pharmacology*
  • Neurotoxins / pharmacology
  • Nitro Compounds
  • Propionates / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Tyrosine 3-Monooxygenase / metabolism

Substances

  • Nerve Growth Factors
  • Neurotoxins
  • Nitro Compounds
  • Propionates
  • Tyrosine 3-Monooxygenase
  • Acetylcholinesterase
  • 3-nitropropionic acid