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首页> 外文期刊>The European Journal of Neuroscience >+)-MCPG induces PKCepsilon translocation in cortical synaptosomes through a PLD-coupled mGluR.
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+)-MCPG induces PKCepsilon translocation in cortical synaptosomes through a PLD-coupled mGluR.

机译：+）-MCPG通过PLD偶联的mGluR诱导皮层突触小体中PKCepsilon易位。

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We have tested whether different agonists of metabotropic glutamate receptors could induce translocation of selective protein kinase C isozymes in nerve terminals. In rat cortical synaptosomes 1S, 3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD; 100 microM) induced an increase in translocation to 124.6 +/- 5.7% of basal unstimulated conditions of the Ca++-independent protein kinase Cepsilon, but not of the Ca++-dependent isozyme beta. This effect was counteracted by 1-aminoindan-1,5-dicarboxylic acid (100 &mgr;M), an antagonist of metabotropic glutamate receptor 1. On the other hand, (+)-alpha-methyl-4-carboxyphenylglycine [(+)-MCPG], an antagonist of metabotropic glutamate receptors group I and II, did not antagonize the effect of 1S,3R-ACPD, and per se induced a translocation of protein kinase Cepsilon of 164 +/- 17.7% of basal unstimulated conditions. Because the (+)-MCPG induction of protein kinase Cepsilon translocation was not antagonized by 1-aminoindan-1, 5-dicarboxylic acid, it is suggested that 1S,3R-ACPD and (+)-MCPG activate this signal transduction pathway through distinct membrane receptors. Indeed (2-[2"-carboxy-3'-phenylcyclopropyl]glycine)-13 (300 nM), a new compound known to antagonize metabotropic glutamate receptors coupled to phospholipase D, was able to antagonize protein kinase Cepsilon translocation induced by (+)-MCPG. Moreover (+)-MCPG directly induced phospholipase D activity, measured as [3H]phosphoethanol production in cortical synaptosomes. These data suggest that in cortical nerve terminals (i) distinct metabotropic glutamate receptors, coupled to different signal transduction pathways, are present, (ii) (+)-MCPG is able to induce protein kinase Cepsilon translocation, and that (iii) a metabotropic glutamate receptor associated to phospholipase D might influence translocation of protein kinase C in a calcium-independent manner.
机译：我们已经测试了代谢型谷氨酸受体的不同激动剂是否可以诱导神经末梢的选择性蛋白激酶C同工酶易位。在大鼠皮层突触小体1S，3R-1-氨基环戊烷-1,3-二羧酸（1S，3R-ACPD; 100 microM）诱导易位增加至不依赖Ca ++的蛋白质的基础未刺激条件的124.6 +/- 5.7％激酶Cepsilon，但不是依赖Ca ++的同工酶β。代谢型谷氨酸受体1的拮抗剂1-氨基茚满-1,5-二羧酸（100μM）可抵消这种作用。另一方面，（+）-α-甲基-4-羧基苯基甘氨酸[（+） -MCPG]，代谢型谷氨酸受体组I和II的拮抗剂，没有拮抗1S，3R-ACPD的作用，并且其本身诱导了蛋白激酶Cepsilon易位，为基础未刺激条件的164 +/- 17.7％。由于蛋白激酶Cepsilon易位的（+）-MCPG诱导不能被1-氨基茚满-1，5-二羧酸拮抗，因此建议1S，3R-ACPD和（+）-MCPG通过不同的途径激活该信号转导途径膜受体。实际上，（2- [2“-羧基-3'-苯基环丙基]甘氨酸）-13（300 nM）是一种新化合物，可拮抗与磷脂酶D偶联的代谢型谷氨酸受体，它能够拮抗由（+ ）-MCPG。此外（+）-MCPG直接诱导磷脂酶D活性，以皮质突触小体中的[3H]磷酸乙醇生成量表示。这些数据表明，在皮质神经末梢（i）不同的代谢型谷氨酸受体与不同的信号转导途径偶联， （ii）（+）-MCPG能够诱导蛋白激酶Cepsilon易位，并且（iii）与磷脂酶D相关的代谢型谷氨酸受体可能以钙非依赖性方式影响蛋白激酶C的易位。

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