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Opiate withdrawal induces dynamic-expressions of AMPA receptors and its regulatory molecule CaMKII alpha in hippocampal synapses

机译：阿片类药物戒断诱导海马突触中AMPA受体及其调节分子CaMKIIα的动态表达

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Adaptive changes in brain areas following drug withdrawal are believed to contribute to drug seeking and relapse. Cocaine withdrawal alters the expression of GluR1 and GluR2/3 subunits of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known. Here, we have examined the expression of GluR1 and GluR2/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent withdrawal. Repeated morphine exposure for 12 d increased GluR1 and GluR2/3 in synaptosome but not in membrane fraction. Interestingly, CaMKII alpha, known to be able to regulate the function of AMPA receptors, was decreased in synaptosome but not in membrane fraction; pCaMKII alpha, the phosphorylated form of CaMKII alpha, was increased in both fractions. However, during opiate withdrawal, GluR1 was generally reduced while GluR2/3 was prominently increased in both fractions; pCaMKII alpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of morphine withdrawal in both fractions. Importantly, the opiate withdrawal-induced increase in GluR2/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP-5 or the antagonist to NR2B-containing NMDA receptors, Ro25-6981. These findings indicate that opiate withdrawal induces dynamic expression of GluR1 and GluR2/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate withdrawal. (c) 2006 Elsevier Inc. All rights reserved.
机译：停药后大脑区域的适应性变化被认为有助于寻找药物和复发。可卡因戒断改变伏伏核或杏仁核中α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体的GluR1和GluR2 / 3亚基的表达，但戒断对海马的影响鲜为人知。在这里，我们检查了吗啡反复接触和随后停药后海马膜和突触部分中GluR1和GluR2 / 3的表达。重复吗啡暴露12天会增加突触体中的GluR1和GluR2 / 3，但不会增加膜部分。有趣的是，已知能够调节AMPA受体功能的CaMKIIα在突触小体中减少了，但在膜部分却没有减少。 pCaMKIIα，CaMKIIα的磷酸化形式，在两个部分中均增加。然而，在鸦片戒断期间，两个部分的GluR1通常降低而GluR2 / 3显着增加。停药后立即使pCaMKIIα强烈降低，但在两个部位的吗啡停药后期均可检测到明显升高。重要的是，阿片类药物戒断诱导的GluR2 / 3的增加取决于糖皮质激素受体和NMDA受体的激活，因为糖皮质激素受体拮抗剂RU38486或海马内注射NMDA受体拮抗剂AP-5或海马拮抗剂可以阻止这种情况。含NR2B的NMDA受体Ro25-6981。这些发现表明阿片戒断诱导海马突触中AMPA受体的GluR1和GluR2 / 3亚基的动态表达，可能揭示了阿片戒断后海马功能的适应性过程。 （c）2006 Elsevier Inc.保留所有权利。

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