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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Calcium influx via ionotropic glutamate receptors causes long lasting inhibition of metabotropic glutamate receptor-coupled phosphoinositide hydrolysis.
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Calcium influx via ionotropic glutamate receptors causes long lasting inhibition of metabotropic glutamate receptor-coupled phosphoinositide hydrolysis.

机译：通过离子型谷氨酸受体的钙流入导致对代谢型谷氨酸受体偶联的磷酸肌醇水解的长期持久抑制。

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摘要

Functional interaction between ionotropic and metabotropic glutamate receptors (iGluR and mGluR respectively) was studied in cerebellar granule cell cultures using quisqualate (QA), the most potent agonist of phosphoinositide hydrolysis coupled mGluR, and N-methyl-D-aspartate (NMDA) or kainate (KA) that activate different classes of iGluR. Two h exposure to NMDA or KA resulted in a marked reduction (about 75%) of QA-evoked PI hydrolysis. The efficacy of the two agonists was about the same, but the potencies were different (IC50 for NMDA about 35 microM and for KA about 70 microM). NMDA-induced depression of QA-stimulated PI hydrolysis was relatively long lasting but reversible. Recovery required protein synthesis. In nominally Ca2+-free medium both NMDA and KA failed to attenuate QA-stimulated PI hydrolysis. The effect of NMDA was prevented by the NMDA receptor antagonist MK801, but not by the wide spectrum protein kinase inhibitor staurosporin nor by the nitric oxide synthase inhibitor N omega-nitro-L-arginine. Cycloheximide and concanavalin A were also ineffective. The effect of KA was prevented by the selective non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX). Voltage sensitive Ca2+ channel antagonists together with MK801 did not counteract the inhibition by KA of the QA response. Both NMDA and KA attenuated PI hydrolysis evoked by the muscarinic receptor agonist carbachol (about 30%), indicating that the activation of iGluRs exerts a relatively general inhibitory effect on the function of different PLC-coupled metabotropic receptors. Consistent with this observation is that treatments either with KA and NMDA induced an inhibition (about 30%) of NaF-stimulated PI hydrolysis which occurs through the direct activation of G proteins. Our observations show that ionotropic glutamate receptor stimulation induces a long lasting suppression of QA-evoked PI breakdown through a Ca2+ dependent mechanism which seems to involve receptor coupled transduction systems downstream from mGluR. Such a Ca2+-dependent cross-talk involving ionotropic and metabotropic receptors may play a role in certain events of synaptic plasticity.
机译：在小脑颗粒细胞培养中，使用quisqualate（QA），磷酸肌醇水解偶联的mGluR和N-甲基-D-天冬氨酸（NMDA）或海藻酸盐作为最有效的激动剂，研究了离子型和代谢型谷氨酸受体（分别为iGluR和mGluR）之间的功能相互作用。 （KA）激活不同类别的iGluR。暴露于NMDA或KA两小时导致QA引发的PI水解显着降低（约75％）。两种激动剂的功效大致相同，但效力不同（NMDA的IC50约为35 microM，KA的IC50约为70 microM）。 NMDA引起的QA刺激的PI水解抑制作用持续时间较长，但可逆。恢复需要蛋白质合成。在名义上不含Ca2 +的培养基中，NMDA和KA均不能减弱QA刺激的PI水解。 NMDA受体拮抗剂MK801阻止了NMDA的作用，但广谱蛋白激酶抑制剂staurosporin或一氧化氮合酶抑制剂Nω-硝基-L-精氨酸均不能阻止NMDA的作用。环己酰亚胺和刀豆球蛋白A也无效。选择性非NMDA受体拮抗剂2,3-二羟基-6-硝基-7-氨磺酰基-苯并（F）喹喔啉（NBQX）阻止了KA的作用。电压敏感的Ca2 +通道拮抗剂与MK801并不能抵消KA对QA反应的抑制作用。毒蕈碱受体激动剂卡巴胆碱（约30％）引起的NMDA和KA均减弱了PI水解，表明iGluRs的活化对不同PLC偶联的代谢型受体的功能具有相对普遍的抑制作用。与该观察结果一致的是，用KA和NMDA处理均可抑制（约30％）NaF刺激的PI水解，这是通过直接激活G蛋白而发生的。我们的观察结果表明，离子型谷氨酸受体刺激通过Ca2 +依赖性机制诱导QA诱发的PI分解的长期抑制，该机制似乎涉及mGluR下游的受体偶联转导系统。这种涉及离子型和代谢型受体的Ca2 +依赖性串扰可能在某些突触可塑性事件中起作用。

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