Activation of group II metabotropic glutamate receptors inhibits glutamate release from salamander retinal photoreceptors
Activation of group II metabotropic glutamate receptors inhibits glutamate release from salamander retinal photoreceptors
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DOI：
10.1017/s0952523802192054
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发表时间：
2002-05-01
影响因子：
1.9
通讯作者：
Lukasiewicz, PD
中科院分区：
文献类型：
--
作者：
Higgs, MH;Lukasiewicz, PD
我们研究了II组代谢型谷氨酸受体（mGluR）激活对蝾螈视网膜切片制备过程中兴奋性突触传递的影响。II组选择性激动剂DCG-IV和LY354740减少神经节细胞的光诱发兴奋性突触后电流（EPSCs）。为了确定这种效应的突触基础，我们还记录了双极细胞和水平细胞。在ON双极细胞中，DCG-IV增加了黑暗时的内向电流，但不影响光照时的峰值电流。在OFF双极细胞和水平细胞中，DCG-IV具有相反的作用，在黑暗中减少向内电流。鉴于这两类突触的极性相反，我们的研究结果表明，II组mGluRs在突触前起作用，减少光感受器的谷氨酸释放。为了确定DCG-IV是否影响视杆细胞或视锥细胞，我们使用光刺激选择性地激活每种类型的光感受器。在水平细胞中，大多数细胞接受来自杆状细胞和视锥细胞的混合突触输入，DCG-IV减少了470 nm刺激诱发的杆状细胞驱动的epsc和在杆状细胞饱和背景下700 nm刺激诱发的锥状细胞驱动的epsc。因此，II组mGluRs的激活减少了杆和锥介导的谷氨酸释放。我们的研究结果表明，II组mGluRs可以介导细胞外谷氨酸抑制谷氨酸从光感受器末端释放的反馈。
We investigated the effects of group II metabotropic glutamate receptor (mGluR) activation on excitatory synaptic transmission in the salamander retinal slice preparation. The group II selective agonists DCG-IV and LY354740 reduced light-evoked excitatory postsynaptic currents (EPSCs) in ganglion cells. To determine the synaptic basis of this effect, we also recorded from bipolar cells and horizontal cells. In ON bipolar cells, DCG-IV increased the inward current in darkness but did not affect the peak current at light onset. In OFF bipolar cells and horizontal cells, DCG-IV had the opposite effect, reducing the inward current in darkness. Given the opposite polarities of these two classes of synapses, our results suggest that group II mGluRs act presynaptically to reduce glutamate release from photoreceptors. To determine whether DCG-IV affected rods or cones, we applied light stimuli that selectively activate each type of photoreceptor. In horizontal cells, most of which receive mixed synaptic input from rods and cones, DCG-IV reduced rod-driven EPSCs evoked by 470-nm stimuli and cone-driven EPSCs elicited by 700-nm stimuli in the presence of a rod-saturating background. Thus, activation of group II mGluRs reduced rod and cone-mediated glutamate release. Our results suggest that group II mGluRs could mediate feedback by which extracellular glutamate inhibits glutamate release from photoreceptor terminals.