Immunohistochemical study on the distribution of insulin-like growth factor I (IGF-I) receptor in the central nervous system of SOD1(G93A) mutant transgenic mice
- Authors
- Chung, YH; Joo, KM; Shin, CM; Lee, YJ; Shin, DH; Lee, KH; Cha, CI
- Issue Date
- Dec-2003
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- amyotrophic lateral sclerosis (ALS); transgenic mice; insulin-like growth factor I (IGF-1) receptor; astrocyte
- Citation
- BRAIN RESEARCH, v.994, no.2, pp 253 - 259
- Pages
- 7
- Journal Title
- BRAIN RESEARCH
- Volume
- 994
- Number
- 2
- Start Page
- 253
- End Page
- 259
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/43839
- DOI
- 10.1016/j.brainres.2003.09.047
- ISSN
- 0006-8993
1872-6240
- Abstract
- In the present study, we used the SOD1(G93A) mutant transgenic mice as an in vivo model of ALS and performed immunohistochemical studies to investigate the changes of insulin-like growth factor I (IGF-I) receptor in the central nervous system. IGF-I receptor-immunoreactive astrocytes were detected in the spinal cord, brainstem, central gray and cerebellar nuclei of SOD1(G93A) transgenic mice. In contrast to transgenic mice, no IGF-I receptor-immunoreactive astrocytes were observed in any brain region of wtSOD1 transgenic mice although a few moderately stained neurons were observed. In the hippocampal formation of SOD1(G93A) transgenic mice, IGF-I receptor immunoreactivity was increased in the pyramidal cells of the CA1-3 regions and granule cells of the dentate gyrus. The present study provides the first evidence that IGF-I receptor immunoreactivity was increased in reactive astrocytes in the central nervous system of SODG93A transgenic mice, suggesting that reactive astrocytes may play an important role in the pathogenesis and progress of ALS. The mechanisms underlying the increased immunoreactivity for IGF-I receptor, and the functional implications of these increases, require elucidation. (C) 2003 Elsevier B.V. All rights reserved.
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