3-Nitropropionic acid-induced changes in bilayer fluidity in synaptosomal membranes: Implications for Huntington's disease

Michael A. LaFontaine, James W. Geddes, D. Allan Butterfield

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


The use of 3-nitropropionic acid (3-NP) and other mitochondria inhibitors to effectuate animal models of Huntington's disease has been well established. 3-NP administration has been shown to lead to pathology similar to that of HD, including massive loss of striatal neurons associated with oxidative stress. Oxidative stress induced by 3-NP also extends to the cortex, an area where little neuron loss occurs. No mechanism as of yet accounts for selective loss of striatal neurons while sparing cortical neurons. In the present study, a nitroxide stearate lipid bilayer-specific spin-label was utilized to probe 3-NP-induced fluidity changes in striatal and cortical synaptosomal membranes. In cortical synaptosomes, membrane fluidity increased in animals previously treated with 3-NP when compared to controls injected with saline vehicle, while in striatal synaptosomes, membrane fluidity decreased in animals treated with 3-NP when compared to controls. The results of the present study suggest that oxidatively-induced changes in membrane fluidity may be involved in mechanisms by which selective striatal neuronal loss occurs in this animal model of Huntington's disease.

Original languageEnglish
Article number376587
Pages (from-to)507-511
Number of pages5
JournalNeurochemical Research
Issue number6
StatePublished - 2002

Bibliographical note

Funding Information:
This work was supported in part by NIH grants to D.A.B. (AG-10836 and AG-05119) and J.W.G. (AG-10836).


  • 3-nitropropionic acid
  • Huntington's disease
  • Membrane lipid fluidity
  • Spin labeling

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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