A non-ionotropic activity of NMDA receptors contributes to glycine-induced neuroprotection in cerebral ischemia-reperfusion injury
| Autor: | Hua-Bao Liao, Qi Wan, Ping Jin, Zhi-Feng Zhang, Rui-Xue Lei, Yu Wan, Juan Chen, Rong Hu, Hua Feng, Ya Zhang, Yang Zhuang |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male Science Glycine Glutamic Acid Pharmacology Neuroprotection Receptors N-Methyl-D-Aspartate Severity of Illness Index Article Brain Ischemia 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Protein Kinase Inhibitors Multidisciplinary Antagonist Strychnine Glycine receptor antagonist medicine.disease Rats Disease Models Animal 030104 developmental biology chemistry nervous system Anesthesia Reperfusion Injury NMDA receptor Medicine Reperfusion injury Proto-Oncogene Proteins c-akt 030217 neurology & neurosurgery Ionotropic effect Protein Binding |
| Zdroj: | Scientific Reports, Vol 7, Iss 1, Pp 1-14 (2017) Scientific Reports |
| ISSN: | 2045-2322 |
| Popis: | NMDA receptor (NMDAR) is known for its ionotropic function. But recent evidence suggests that NMDAR also has a non-ionotropic property. To determine the role of non-ionotropic activity of NMDARs in clinical relevant conditions, we tested the effect of glycine, a co-agonist of NMDARs, in rat middle cerebral artery occlusion (MCAO), an animal model of cerebral ischemia-reperfusion injury after the animals were injected with the NMDAR channel blocker MK-801 and the glycine receptor antagonist strychnine. We show that glycine reduces the infarct volume in the brain of ischemic stroke animals pre-injected with MK-801 and strychnine. The effect of glycine is sensitive to the antagonist of glycine-GluN1 binding site and blocked by Akt inhibition. In the neurobehavioral tests, glycine improves the functional recovery of stroke animals pre-injected with MK-801 and strychnine. This study suggests that glycine-induced neuroprotection is mediated in part by the non-ionotropic activity of NMDARs via Akt activation in cerebral ischemia-reperfusion injury. |
| Databáze: | OpenAIRE |
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