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Objective To explore the dynamic changes of glutamate in the cortex of cynomolgus monkeys during cerebral ischemia.Methods Proximal M1 segment of middle cerebral artery (MCA) was occluded for 1 h in 3 young cynomolgus monkeys (7.3 ± 1.5 years old) to induce cerebral ischemia.Magnetic resonance imaging and neurologic deficit scoring were used to evaluate the ischemia and observe the manifestations,respectively.Fast Analytical Sensing Technology (FAST) was applied to record the content of cortex glutamate in the same site of ipsilateral primary motor cortex in the periods of pre-,during,and post-occlusion,and at 1 and 2 weeks after surgery.Results Compared with pre-occlusion,the content of glutamate was increased significantly in the process of occluding in the MCA M1 (P =0.003);No significant difference was observed in the content during occluding and post-occlusion (P--0.877).The content in the first week was decreased obviously as compared with post-occlusion (P--0.004),but it showed no statistical difference with that in the second week (P =0.085).Conclusion Cerebral ischemia may potentially accelerate the extra-cellular glutamate release in the cortex,but reperfusion may ameliorate or balance off the glutamate release.
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Objective:To determine the neuroprotective effect of ginkgolides(Gin)on cultured rat embryos dorsal root ganglion(DRG)neurons injured by glutamate(Glu)in vitro.Methods:DRG neurons of Wistar rat embryos were cultured in vitro for 48 h and then exposed to Glu(200 μmol/L)with or without Gin(50 μmol/L).The living cells were observed with an inverted contrast microscope.The cultures were processed for detecting the apoptosis rate by using flow cytometry.The fluorescent intensity of intracellular Ca2+ was detected by confocal laser scanning microscope(CLSM).Results:The living status of DRG cells with Gin incubation was better than that of incubated cultures without Gin.The shape of neuronal cell bodies or neurite networks were almost the same in the glutamic acid group with Gin compared with that of the normal control group.The apoptosis rate of cells incubated with Glu for 24 h was 41.1% in DRG cultures.The apoptosis rate of cells incubated with Glu and 50 μmol/L of Gin for 24 h was 7.6% in DRG cultures.The fluorescent intensity was lower in Gin with Glu group than that in Glu group(P＜0.01).The fluorescent intensity was lower in the control group than that in Glu group(P＜0.01).There was no significant difference in the fluorescent intensity between Gin with Glu group and control group(P＞0.05).Conclusion:Ginkgolides may reduce intracellular Ca2+ concentration,and then protect DRG neurons from neurotoxicity induced by Glu.
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Objective To study the effect of baicalin on the content of glutamate acid (Glu), aspartic acid (Asp), ?-aminobutyric acid (GABA) in the brain of rat with experimental intracerebral hemorrhage. Methods The intracerebral hemorrhage rat model was induced by collagen enzyme + heparin sodium. The rats were randomly divided into sham group, model group and high, middle, low dose group of baicalin. Rats were treated with the physiological saline and different concentration of baicalin respectively. The brain of each group was taken out three days later and the brain homogenate was prepared. The content of Glu, Asp and GABA was measured with the high performance liquid chromatography (HPLC). Results Compared with the sham group, the levels of Asp were obviously higher (P0.05) in each dose group of baicalin. Compared with the sham group, the contents of Glu were increased obviously (P
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@#ObjectiveTo investigate the protective effect of LY367385 on impairment of cultured mouse cerebral cortical neurons induced by sodium glutamate (Glu) or oxygen-glucose deprivation (OGD).MethodsNeuron damage induced by Glu or OGD, as well as the action of (S)-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385) were measured by determining the leakage of lactate dehydrogenase (LDH) from neurons. Immunocytochemistry and immunofluorescent methods were used to detect the expression of anti-mGluR1α. Morphological observation of primary cortical neurons was performed by phase contrast microscope.ResultsFollowing the exposure to 0.1 mmol/L Glu for 1 h or OGD for 1 h, LDH leakage from neurons obviously increased (P< 0.01 ). 50 mmol/L LY367385, when co-incubated with Glu or OGD, markedly reduced the LDH leakage (P<0.01). The 24-h leakage of LDH was increased from cells exposed to 0.1 mmol/L Glu for 15 min. Pre-and post-treatment with LY367385 (50 mmol/L ) decreased the leakage of LDH. The cultured neurons expressed mGluR1α.ConclusionLY367385 has protective effect on neurons damaged by Glu or OGD. It may be related to antagonizing mGluR1α.