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首页> 外文期刊>The European Journal of Neuroscience >Depression of GABAergic input to identified hippocampal neurons by group III metabotropic glutamate receptors in the rat.
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Depression of GABAergic input to identified hippocampal neurons by group III metabotropic glutamate receptors in the rat.

机译：大鼠中III组代谢型谷氨酸受体对识别的海马神经元的GABA能输入的抑制作用。

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摘要

Abstract The release of GABA in synapses is modulated by presynaptic metabotropic glutamate receptors (mGluRs). We tested whether GABA release to identified hippocampal neurons is influenced by group III mGluR activation using the agonist L-(+)-2-amino-4-phosphonobutyric acid (L-AP4) on inhibitory postsynaptic currents (IPSCs) evoked in CA1 interneurons and pyramidal cells. In interneurons, characterized with biocytin and immunolabelling for somatostatin, evoked IPSCs were depressed by 50 micro m L-AP4 (activating mGluR4 and 8) to 68 +/- 6% of control, but they were rarely depressed in pyramidal cells (96 +/- 4% of control). At 300-500 micro m concentration (activating mGluR4, 7 and 8), L-AP4 depressed IPSCs in both interneurons (to 70 +/- 6%) and pyramidal cells (to 67 +/- 4%). The change in trial-to-trial variability and in paired-pulse depression indicated a presynaptic action. In interneurons, the degree of IPSC depression was variable (to 9-87%), and a third of IPSCs were not affected by L-AP4. The L-AP4-evoked IPSC depression was blocked by LY341495. The depression of IPSCs was similar in O-LM cells and other interneurons. The lack of cell-type selectivity and the similar efficacy of different concentrations of L-AP4 suggest that several group III mGluRs are involved in the depression of IPSCs. Electron microscopic immunocytochemistry confirmed that mGluR4, mGluR7a and mGluR8a occur in the presynaptic active zone of GABAergic terminals on interneurons, but not on those innervating pyramidal cells. The high variability of L-AP4-evoked IPSC suppression is in line with the selective expression of presynaptic mGluRs by several distinct types of GABAergic neuron innervating each interneuron type.
机译：摘要突触前代谢型谷氨酸受体（mGluRs）调节突触中GABA的释放。我们测试了激动剂L-（+）-2-氨基-4-膦酸丁酸（L-AP4）对CA1间神经元中引起的抑制性突触后电流（IPSC）的作用，III组mGluR活化是否影响了GABA释放至已识别的海马神经元。锥体细胞。在以生物周期蛋白和生长抑素免疫标记为特征的中间神经元中，诱发的IPSC被50微米L-AP4（激活mGluR4和8）抑制至对照组的68 +/- 6％，但在锥体细胞中很少被抑制（96 + / -控制的4％）。在300-500微米的浓度下（激活mGluR4、7和8），L-AP4抑制了中间神经元（至70 +/- 6％）和锥体细胞（至67 +/- 4％）中的IPSC。试验间差异和成对脉冲抑制的变化表明突触前的作用。在中间神经元中，IPSC抑郁的程度是可变的（9-87％），并且三分之一的IPSC不受L-AP4的影响。 L-AP4引起的IPSC抑制被LY341495阻止。 OSC-LM细胞和其他中间神经元的IPSC抑制相似。缺乏细胞类型的选择性以及不同浓度的L-AP4的相似功效表明，几种IIImGluRs参与了IPSC的抑制。电子显微镜免疫细胞化学证实，mGluR4，mGluR7a和mGluR8a发生在中间神经元上的GABA能端的突触前活动区，而不是在那些支配的锥体细胞上。 L-AP4引起的IPSC抑制的高变异性与神经中枢神经元类型的几种不同类型的GABA能神经元对突触前mGluRs的选择性表达相一致。

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