Higgs M H, Romano C, Lukasiewicz P D
Neuroscience Program, Department of Ophthalmology and Visual Science, Washington University School of Medicine, Campus Box 8096, 660 S Euclid Avenue, St. Louis, MO 63110, USA.
Neuroscience. 2002;115(1):163-72. doi: 10.1016/s0306-4522(02)00381-0.
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.
代谢型谷氨酸受体（mGluRs）位于视网膜的两个神经纤维层中，可能调节光感受器与双极细胞之间以及双极细胞与神经节细胞之间的信号传递。我们研究了mGluR激活是否调节蝾螈视网膜切片标本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-膦酰丁酸（AP4）抑制电刺激诱发的神经节细胞单突触兴奋性突触后电流（EPSCs），而I组和II组激动剂则无显著作用。AP4降低了神经节细胞微小EPSCs的频率但不影响其幅度，提示在双极细胞终末存在突触前作用。AP4还降低了光刺激偏移诱发的神经节细胞EPSCs，提示III组mGluRs调节来自OFF双极细胞的递质释放。比较OFF双极细胞和神经节细胞中光诱发的EPSCs表明，AP4主要通过作用于双极细胞终末来降低神经节细胞EPSCs，对光感受器终末的作用较小。II/III组mGluR拮抗剂（RS）-α-环丙基-4-膦酰苯甘氨酸（CPPG）阻断了AP4在双极细胞终末的作用，这与III组mGluRs在这些部位的定位一致。然而，CPPG在光偏移时并未增加EPSCs，表明突触谷氨酸对III组mGluRs的激活在调节从双极细胞到神经节细胞的信号传递中作用不大。
