Chronic stress induces opposite changes in the mRNA expression of the cell adhesion molecules NCAM and L1

被引:93
作者
Venero, C
Tilling, T
Hermans-Borgmeyer, I
Schmidt, R
Schachner, M
Sandi, C
机构
[1] Univ Nacl Educ Distancia, Dept Psychobiol, Madrid 28040, Spain
[2] Univ Hamburg, Zentrum Mol Neurobiol, D-20246 Hamburg, Germany
[3] Univ Giessen, Zentrum Biotech Betriebseinheit, D-35392 Giessen, Germany
关键词
stress; NCAM; L1; learning; neural plasticity;
D O I
10.1016/S0306-4522(02)00543-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The effects of 21-day exposure to restraint stress on mRNA levels of the cell adhesion molecules NCAM and L1 were evaluated in different hippocampal regions (CA1, CA3, and dentate gyrus) and other structures (thalamus, prefrontal and frontal cortices, and striatum) of the rat brain. A general decrease in gene expression of the neural cell adhesion molecule (NCAM) was found throughout the brain, particularly in all hippocampal subregions. On the contrary, transcripts for the adhesion molecule L1 were specifically increased at the level of the hippocampus, especially in the dorsal dentate gyrus and area CA3. mRNA for the NCAM180 isoform was detected unchanged in all brain areas examined after chronic stress. A second experiment explored whether there would be cognitive alterations associated with this stress procedure and molecular regulation. Thus, after exposure to the same restraint regimen, performance in the water maze was evaluated. Although stressed rats displayed the ability to learn the task throughout the training session, they showed a transient deficit in the initial phase of the acquisition. In conclusion, our findings indicate that chronic stress interferes with the mechanisms involved in the synthesis of cell adhesion molecules of the immunoglobulin superfamily. Furthermore, they suggest that these effects might be involved in the mechanisms by which stress induces structural and functional alterations in the central nervous system and, particularly, in the hippocampus. (C) 2002 IBRO. Published by Elsevier Science Ltd, All rights reserved.
引用
收藏
页码:1211 / 1219
页数:9
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