Kainate receptor-mediated synaptic currents in cerebellar Golgi cells are not shaped by diffusion of glutamate
Kainate receptor-mediated synaptic currents in cerebellar Golgi cells are not shaped by diffusion of glutamate
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DOI：
10.1073/pnas.97.12.6838
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发表时间：
2000-06-06
影响因子：
11.1
通讯作者：
Mulle, C
中科院分区：
文献类型：
--
作者：
Bureau, I;Dieudonné, S;Mulle, C
我们报告存在红藻氨酸受体（KARs）在小脑高尔基体细胞的野生型，但不是GluR 6缺陷型小鼠。平行纤维刺激激活KAR介导的小幅度突触电流[KAR-兴奋性突触后电流（EPSC）]。KAR-EPSC与α-氨基-3-羟基-5-甲基异恶唑-4-丙酸酯（AMPA）受体介导的突触电流（AMPAR-EPSC）在同一突触上有很大不同。KAR-EPSC显示缓慢的上升和衰减时间，并响应于一系列刺激而累加。使用PDA。一种低亲和力的竞争性拮抗剂和修改谷氨酸清除率的药物，我们发现这些特性不能用谷氨酸在突触间隙外的扩散和突触外KARs的激活来解释。这些数据表明，KAR-EPSC的缓慢动力学是由于KAR的内在属性被定位在突触后位点。KAR-和AMPAR-EPSC在动力学和求和方面的对比特性为突触能突触整合两个不同时间尺度的兴奋性输入提供了可能性。
We report the presence of kainate receptors (KARs) in cerebellar Golgi cells of wild-type but not GluR6-deficient mice. Parallel fiber stimulation activates KAR-mediated synaptic currents [KAR-excitatory postsynaptic currents (EPSCs)] of small amplitude. KAR-EPSCs greatly differ from synaptic currents mediated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AM PA) receptors (AMPAR-EPSCs) at the same synapse. KAR-EPSCs display slow rise and decay time and summate in response to a train of stimulations. By using PDA. a low-affinity competitive antagonist and agents that modify the clearance of glutamate, we show that these properties cannot be explained by diffusion of glutamate outside of the synaptic cleft and activation of extrasynaptic KARs. These data suggest that the slow kinetic of KAR-EPSCs is due to intrinsic properties of KARs being localized at postsynaptic sites, The contrasting properties of KAR- and AMPAR-EPSCs in terms of kinetics and summation offer the possibility for a glutamatergic synapse to integrate excitatory inputs over two different time scales.