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首页> 外文期刊>Neuropharmacology >The role of NMDA receptors in regulating group II metabotropic glutamate receptor-mediated long-term depression in rat medial prefrontal cortex.
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The role of NMDA receptors in regulating group II metabotropic glutamate receptor-mediated long-term depression in rat medial prefrontal cortex.

机译：NMDA受体在调节大鼠内侧前额叶皮层的II型代谢型谷氨酸受体介导的长期抑郁中的作用。

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Previous work has shown that brief application of group II metabotropic glutamate receptor (mGluR) agonist (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl) glycine (DCG-IV) can induce long-term depression (LTD) of excitatory transmission on layer V pyramidal neurons of rat medial prefrontal cortex (mPFC). An unusual feature of this LTD is that it relies on activation of both group II mGluRs and N-methyl-d-aspartate receptors (NMDARs). However, it is not known whether other specific group II mGluR agonists also induce LTD and whether they depend on the conjoint activation of group II mGluRs and NMDARs. We show here that the ability of DCG-IV to induce LTD was mimicked by a more selective group II mGluR agonist, LY379268. The induction of LTD by a lower concentration of DCG-IV (0.2muM) or LY379268 (0.03muM) was blocked by the NMDAR antagonist APV or the interruption of synaptic stimulation during drug application. In contrast, application of a higher concentration of DCG-IV (1muM) or LY379268 (0.1muM) can induce LTD that was independent of synaptic NMDAR activation. These results suggest that although molecular cooperation between group II mGluRs and synaptic NMDARs may facilitate the induction of group II mGluR-mediated LTD at excitatory synapses onto mPFC layer V pyramidal neurons, enhancing group II mGluR activation may remove NMDAR involvement in this form of synaptic plasticity.
机译：先前的研究表明，对II组代谢型谷氨酸受体（mGluR）激动剂（2S，2'R，3'R）-2-（2'，3'-二羧基环丙基）甘氨酸（DCG-IV）的简要应用可诱导大鼠内侧前额叶皮层（mPFC）的V层锥体神经元上的兴奋性传递的长期抑郁症（LTD）。该LTD的一个不寻常的特征是它依赖于II型mGluRs和N-甲基-d-天冬氨酸受体（NMDARs）的激活。但是，尚不清楚其他特定的II型mGluR激动剂是否也诱导LTD，以及它们是否依赖于II型mGluRs和NMDAR的联合激活。我们在这里显示，DCG-IV诱导LTD的能力被更具选择性的II型mGluR激动剂LY379268模仿。 NMDAR拮抗剂APV阻止了较低浓度DCG-IV（0.2μM）或LY379268（0.03μM）对LTD的诱导，或在药物应用过程中中断了突触刺激。相反，施加更高浓度的DCG-IV（1μM）或LY379268（0.1μM）可以诱导LTD，其独立于突触NMDAR激活。这些结果表明，尽管II组mGluR和突触NMDAR之间的分子合作可能促进在兴奋性突触上将II组mGluR介导的LTD诱导到mPFC层V锥体神经元上，但增强II组mGluR的激活可能会消除NMDAR参与这种形式的突触可塑性。

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