国家神经系统疾病临床医学研究中心数据管理与共享系统

Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases

Blood-Based Glutamate Scavengers Reverse Traumatic Brain Injury-Induced Synaptic Plasticity Disruption by Decreasing Glutamate Level in Hippocampus Interstitial Fluid, but Not Cerebral Spinal Fluid, In Vivo

第一作者:Zhang Dainan

通讯作者:Jia Wang

Glutamate-oxaloacetate transaminase Hippocampus Lo

基本信息

  • 负责人:Zhang Dainan
  • 数据来源: OTHERS
  • 论文编号:OTHERS20190665
  • 发表时间:2019-02-01

2019-02-01

已发表文章

发表杂志:Neurotox Res

发表类型: Original Article

影响因子(IF): 3.911

PMID: 30255425 Pubmed原文链接 全文下载

主要研究背景及目的

方法

Acutely promoting brain glutamate clearance with a blood-based scavenging system, glutamate oxaloacetate transaminase (GOT), prevents the delayed inhibition of LTP post-TBI. Here, we report that repeated dosing of recombinant GOT type 1, with the glutamate co-substrate oxaloacetate, could induce a persistent enhancement of serum level of GOT and reverse the disruption of synaptic plasticity 4 days after the induction of TBI in rats.

结论

Overall, the present findings support the importance of clearance of glutamate post-TBI and provide new evidence of the mechanism of glutamate-induced LTP inhibition which leads to a development of evaluations, intervention, and reversion for post-TBI cognitive deficit.

主要结果

Moreover, the change of glutamate level post-TBI presents a different timeframe in ventricular CSF and hippocampus interstitial fluid (ISF), and the application of rGOT may reverse the inhibition of LTP by decreasing the glutamate level in hippocampus ISF, but not ventricular CSF. Lastly, we found that the intervention did not significantly affect the total level of glutamate in the hippocampus as well as the expression of major glutamate transporters, EAAT1 and EAAT2.