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3-nitropropionic acid-induced changes in bilayer fluidity in synaptosomal membranes: implications for Huntington's
Michael A LaFontaine1, James W Geddes, D Allan Butterfield
1Department of Chemistry, Central Connecticut State University, New Britain, Connecticut 06050, USA.
Neurochemical Research
|August 30, 2002
Summary
3-nitropropionic acid (3-NP) induces Huntington's disease-like pathology. This study found 3-NP alters membrane fluidity differently in striatal and cortical neurons, suggesting a mechanism for selective neuronal loss.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- 3-nitropropionic acid (3-NP) is used to model Huntington's disease (HD) in animals.
- 3-NP causes oxidative stress and striatal neuron loss, but the mechanism for selective vulnerability is unknown.
Purpose of the Study:
- To investigate if 3-NP-induced changes in synaptosomal membrane fluidity contribute to selective striatal neuron loss in an HD animal model.
Main Methods:
- Utilized a nitroxide stearate spin-label to measure membrane fluidity in striatal and cortical synaptosomes.
- Compared membrane fluidity in 3-NP treated animals versus saline-injected controls.
Main Results:
- In cortical synaptosomes, 3-NP treatment increased membrane fluidity compared to controls.
- In striatal synaptosomes, 3-NP treatment decreased membrane fluidity compared to controls.
Conclusions:
- Oxidatively-induced alterations in membrane fluidity may play a role in the selective loss of striatal neurons observed in 3-NP-induced models of Huntington's disease.