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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Presynaptic effects of group III metabotropic glutamate receptors on excitatory synaptic transmission in the retina.
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Presynaptic effects of group III metabotropic glutamate receptors on excitatory synaptic transmission in the retina.

机译:第三类代谢型谷氨酸受体对视网膜兴奋性突触传递的突触前作用。

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Metabotropic glutamate receptors (mGluRs) are located in both plexiform layers in the retina and may modulate transmission between photoreceptors and bipolar cells and between bipolar and ganglion cells. We investigated whether mGluR activation modulates excitatory synaptic input to bipolar cells and ganglion cells in the salamander retinal slice preparation. The group III mGluR agonist L-2-amino-4-phosphonobutyric acid (AP4) inhibited monosynaptic excitatory postsynaptic currents (EPSCs) in ganglion cells evoked by electrical stimuli, whereas group I and group II agonists had no significant effect. AP4 reduced the frequency but not the amplitude of ganglion cell miniature EPSCs, suggesting a presynaptic action at bipolar cell terminals. AP4 also reduced ganglion cell EPSCs evoked by the offset of a light stimulus, suggesting that group III mGluRs modulate release from OFF bipolar cells. Comparison of light-evoked EPSCs in OFF bipolar cells and ganglion cells indicated that AP4 reduced ganglion cell EPSCs by acting primarily at bipolar cell terminals, and to a lesser extent at photoreceptor terminals. The group II/III mGluR antagonist (RS)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG) blocked the effect of AP4 at bipolar cell terminals, consistent with localization of group III mGluRs at these sites. However, CPPG did not increase EPSCs at light offset, indicating that activation of group III mGluRs by synaptic glutamate does not play a large role in modulating transmission from bipolar cells to ganglion cells.
机译:代谢型谷氨酸受体(mGluRs)位于视网膜的两个丛状层中,并且可以调节感光细胞与双极细胞之间以及双极与神经节细胞之间的传递。我们调查了mGluR激活是否调节sal视网膜切片制备中双极细胞和神经节细胞的兴奋性突触输入。 III组mGluR激动剂L-2-氨基-4-膦酰基丁酸(AP4)抑制电刺激诱发的神经节细胞中的单突触兴奋性突触后突触电流(EPSC),而I组和II组激动剂则无明显作用。 AP4降低了神经节细胞微型EPSC的频率,但没有降低幅度,表明在双极细胞末端有突触前作用。 AP4还减少了由光刺激的抵消引起的神经节细胞EPSC,这表明IIImGluRs调节了OFF双极细胞的释放。 OFF双极细胞和神经节细胞中的光诱发EPSC的比较表明,AP4通过主要作用于双极细胞末端,并在较小程度上作用于感光细胞末端,降低了神经节细胞EPSC。 II / III组mGluR拮抗剂(RS)-α-环丙基-4-膦酰基苯基甘氨酸(CPPG)阻断了AP4在双极细胞末端的作用,这与IIIG组mGluRs在这些位点的定位一致。但是,CPPG不会在光偏​​移时增加EPSC,这表明突触谷氨酸对IIImGluRs的激活在调节双极细胞向神经节细胞的传递中不起很大作用。

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