TY - T1的腺苷,负责互动/ A1受体介导调制谷氨酸释放的机制引起的瞬态小鼠局灶性脑缺血神经学(P06.223) JF -乔-神经病学SP - P06.223 LP - P06.223六世- 78 - 1补充非盟-李Gui盟Hao-Xiang王盟文汇风扇李盟-刘本盟Chuan-Ming Y1 - 2012/04/26 UR - http://n.neurol首页ogy.org/content/78/1_Supplement/P06.223.abstract N2 -目的:负责/ A1受体交叉交互影响和A1受体激活活动增强了抑制兴奋性毒性的淘汰赛,负责受体小鼠缺血大脑。在大脑缺血性背景细胞外腺苷水平提高。负责受体失活显著减少,负责受体基因小鼠的脑损伤。过去的研究显示没有直接抑制谷氨酸释放通过阻断受体负责但前提是A1受体被激活。设计/方法:MCAO /再灌注模型中创建负责受体淘汰赛(KO)及其野生型小鼠(WT)控制。有三组:各组,A1受体激活剂治疗,A1拮抗剂治疗。观察神经功能的改变在A1受体刺激或灭活。mRNA水平A1受体和转运体谷氨酸(GLT-1)缺血区(免疫印迹和rt - pcr)检测。所有数据用SPSS 13.0软件进行了分析。Mann-Whitney U测试是用来比较神经赤字。结果:1。负责受体基因敲除可以升级A1受体表达。2。 Ischemic neuroprotection of A2AR deficiency is related to the activation of A1 receptor If untreated, in both A1 antagonist and A1 receptor activator treated group, the neurological deficit scores were lower in KO mice than in WT mice(P<0.05 and P<0.01). In the A1 antagonist treated group, deficit scores were remarkably higher than in both KO and WT mice(p<0.05). In the presence of A1 receptor stimulator, deficit scores were remarkably lower than those in both KO and WT mice (p<0.05). 3. A1 receptor enhances GLT-1 expression.Conclusions: The neuroprotection after blocking A2A receptor in ischemic condition is via enhancing the function of the GLT-1 to transport glutamate from extracellular to intracellular space. By up-regulating A1 receptor function, glutamate and its receptor mediated excitatory toxicity have been inhibited. Our research clarified the molecular mechanism of ischemic neuroprotection after A2A receptor has been inhibited.Disclosure: Dr. Gui has nothing to disclose. Dr. Li has nothing to disclose. Dr. Li has nothing to disclose. Dr. Li has nothing to disclose. Dr. Li has nothing to disclose.Thursday, April 26 2012, 07:30 am-12:00 pm ER -