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NMDA-induced increases in rat brain glutamine synthetase but not glial fibrillary acidic protein are mediated by free radicals
| Content Provider | Semantic Scholar |
|---|---|
| Author | Jones, Jane Davenport Atterwill, Christopher Kenneth |
| Copyright Year | 1998 |
| Abstract | Both excitotoxicity and oxidative stress are implicated in the pathophysiology of central nervous system (CNS) ischaemia-reperfusion injury whereby astrocytes offer neural protection through the production of endogenous antioxidants and removal of glutamate from the extracellular milieu. This study investigated whether exogenous alpha-tocopherol, an antioxidant, could prevent N-methyl-D-aspartate (NMDA)-produced increases of the glial specific proteins, glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP) in rat brain spheroids in vitro. NMDA (320 microM; 3 days in vitro (DIV)) was unable to induce lipid peroxidation in rat brain spheroids implying that excitotoxicity in this system did not involve substantial free radical formation. However at non-cytotoxic concentrations, increases in astroglial GS were prevented by alpha-tocopherol treatment, suggesting a role for ROS in the excitotoxic process. In contrast, NMDA-induced increases in GFAP remained unchanged by alpha-tocopherol indicating that oxidative stress may not be involved in reactive gliosis at non-cytotoxic NMDA concentrations. |
| Starting Page | 37 |
| Ending Page | 40 |
| Page Count | 4 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/S0304-3940(98)00285-7 |
| PubMed reference number | 9637404 |
| Journal | Medline |
| Volume Number | 247 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0304394098002857 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0304394098002857?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/S0304-3940%2898%2900285-7 |
| Journal | Neuroscience Letters |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
