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Spectroscopy: An International Journal
Volume 27, Article ID 176937, 10 pages
http://dx.doi.org/10.1155/2012/176937

Synchrotron FTIR Microspectroscopy Study of the Striatum in 6-Hydroxydopamine Rat Model of Parkinson's Disease

1Laboratory of Neuropharmacology and Neurotoxicology, School of Life Sciences, Shanghai University, Nanchen Road 333, Shanghai 200436, China
2Shanghai Key Laboratory of Special Artificial Microstructure Materials and Technology, Physics Department, Tongji University, Shanghai 200092, China
3National Synchrotron Radiation Laboratory, USTC, Hefei 230026, China

Copyright © 2012 Zhu Hongyan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In the present study, synchrotron-based Fourier transform-infrared (FTIR) microspectroscopy is used to analyze the biochemical composition of the striatal neurons in normal and Parkinson's disease (PD) rat brain tissues. The rat model of Parkinson's disease is established by destroying the nigrostriatal pathway with 6-hydroxydopamine (6-OHDA). The detailed spectral analyses show the significant changes of cellular compositions such as lipids, and proteins in the striatal neurons of 6-OHDA-lesioned PD rats with respect to control neurons. As a result, the intensities of spectral absorption assigned to lipid of the striatal neurons in PD rats are higher than in control animals. Furthermore, the unsaturation levels of phospholipids decrease in PD neurons with respect to control neurons, indicating a high level of lipid peroxidation. The analysis of protein secondary structure shows the significantly higher ratio of 𝛽 -sheet in PD neurons compared to that of control neurons, suggesting that the abnormal protein structure occurs before their morphological appearances in the striatal neurons. These findings suggest that the biochemical changes in neurons could be involved in the pathogenesis of Parkinson's disease.