期刊
NEUROCHEMICAL RESEARCH
卷 33, 期 11, 页码 2318-2323出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-008-9731-8
关键词
excitotoxicity; neuroinflammation; interleukin-1beta; tumor necrosis factor alpha; interleukin-10; glial fibrillary acidic protein; inducible nitric oxide synthase; brain
资金
- Intramural Research Program of the National Institute on Aging, National Institutes of Health
Chronic N-Methyl-D-aspartate (NMDA) administration, a model of excitotoxicity, and chronic intracerebroventricular lipopolysaccharide infusion, a model of neuroinflammation, are reported to upregulate arachidonic acid incorporation and turnover in rat brain phospholipids as well as enzymes involved in arachidonic acid metabolism. This suggests cross-talk between signaling pathways of excitotoxicity and of neuroinflammation, involving arachidonic acid. To test whether chronic NMDA administrations to rats can upregulate brain markers of neuroinflammation, NMDA (25 mg/kg i. p.) or vehicle (1 ml saline/kg i. p.) was administered daily to adult male rats for 21 days. Protein and mRNA levels of cytokines and other inflammatory markers were measured in the frontal cortex using immunoblot and realtime PCR. Compared with chronic vehicle, chronic NMDA significantly increased protein and mRNA levels of interleukin-1beta, tumor necrosis factor alpha, glial fibrillary acidic protein and inducible nitric oxide synthase. Chronic NMDA receptor overactivation results in increased levels of neuro-inflammatory markers in the rat frontal cortex, consistent with cross-talk between excitotoxicity and neuroinflammation. As both processes have been reported in a number of human brain diseases, NMDA receptor inhibitors might be of use in treating neuroinflammation in these diseases.
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