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I 型和 II 型代谢型谷氨酸受体的激活均可抑制视网膜节细胞向外侧膝状体的传递。

Activation of both Group I and Group II metabotropic glutamatergic receptors suppress retinogeniculate transmission.

机构信息

University of Chicago, Department of Neurobiology, 947 E. 58th Street, Chicago, IL 60637, United States.

出版信息

Neuroscience. 2013 Jul 9;242:78-84. doi: 10.1016/j.neuroscience.2013.03.043. Epub 2013 Apr 1.

DOI:10.1016/j.neuroscience.2013.03.043
PMID:23558090
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3654074/
Abstract

Relay cells of dorsal lateral geniculate nucleus (LGN) receive a Class 1 glutamatergic input from the retina and a Class 2 input from cortical layer 6. Among the properties of Class 2 synapses is the ability to activate metabotropic glutamate receptors (mGluRs), and mGluR activation is known to affect thalamocortical transmission via regulating retinogeniculate and thalamocortical synapses. Using brain slices, we studied the effects of Group I (dihydroxyphenylglycine) and Group II ((2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine) mGluR agonists on retinogeniculate synapses. We showed that both agonists inhibit retinogeniculate excitatory postsynaptic currents (EPSCs) through presynaptic mechanisms, and their effects are additive and independent. We also found high-frequency stimulation of the layer 6 corticothalamic input produced a similar suppression of retinogeniculate EPSCs, suggesting layer 6 projection to LGN as a plausible source of activating these presynaptic mGluRs.

摘要

背外侧膝状体核(LGN)的中继细胞接收来自视网膜的 1 类谷氨酸能输入和来自皮质 6 层的 2 类输入。2 类突触的特性之一是能够激活代谢型谷氨酸受体(mGluRs),并且已知 mGluR 的激活通过调节视网膜神经节和丘脑皮质突触来影响丘脑皮质传递。使用脑切片,我们研究了 I 组(二羟苯甘氨酸)和 II 组((2S,2'R,3'R)-2-(2',3'-二羧基环丙基)甘氨酸)mGluR 激动剂对视网膜神经节兴奋性突触后电流(EPSC)的影响。我们表明,两种激动剂均通过突触前机制抑制视网膜神经节 EPSC,其作用是相加且独立的。我们还发现,6 层皮质丘脑传入的高频刺激产生了类似的视网膜神经节 EPSC 抑制,这表明 6 层向 LGN 的投射可能是激活这些突触前 mGluRs 的来源。

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