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BioMed Research International
Volume 2014, Article ID 498410, 11 pages
Research Article

Proteomic Identification of Altered Cerebral Proteins in the Complex Regional Pain Syndrome Animal Model

1Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnam 463707, Republic of Korea
2School of Life Science, Gwangju Institute of Science and Technology, Gwangju 500712, Republic of Korea
3Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 143701, Republic of Korea
4Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul 110744, Republic of Korea

Received 6 March 2014; Revised 14 August 2014; Accepted 25 August 2014; Published 16 September 2014

Academic Editor: Livio Luongo

Copyright © 2014 Francis Sahngun Nahm 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.


Background. Complex regional pain syndrome (CRPS) is a rare but debilitating pain disorder. Although the exact pathophysiology of CRPS is not fully understood, central and peripheral mechanisms might be involved in the development of this disorder. To reveal the central mechanism of CRPS, we conducted a proteomic analysis of rat cerebrum using the chronic postischemia pain (CPIP) model, a novel experimental model of CRPS. Materials and Methods. After generating the CPIP animal model, we performed a proteomic analysis of the rat cerebrum using a multidimensional protein identification technology, and screened the proteins differentially expressed between the CPIP and control groups. Results. A total of 155 proteins were differentially expressed between the CPIP and control groups: 125 increased and 30 decreased; expressions of proteins related to cell signaling, synaptic plasticity, regulation of cell proliferation, and cytoskeletal formation were increased in the CPIP group. However, proenkephalin A, cereblon, and neuroserpin were decreased in CPIP group. Conclusion. Altered expression of cerebral proteins in the CPIP model indicates cerebral involvement in the pathogenesis of CRPS. Further study is required to elucidate the roles of these proteins in the development and maintenance of CRPS.