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首页> 外文期刊>The European Journal of Neuroscience >Differential role of mGlu1 and mGlu5 receptors in rat hippocampal slice models of ischemic tolerance.
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Differential role of mGlu1 and mGlu5 receptors in rat hippocampal slice models of ischemic tolerance.

机译：mGlu1和mGlu5受体在大鼠海马切片缺血耐受模型中的差异作用。

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Activation of glutamate receptors has been proposed as a key factor in the induction of ischemic tolerance. We used organotypic rat hippocampal slices exposed to 30 min oxygen-glucose deprivation (OGD) to evaluate postischemic pyramidal cell death in the CA1 subregion. In this model, 10 min exposure to OGD 24 h before the exposure to toxic OGD was not lethal and reduced the subsequent OGD neurotoxicity by approximately 53% (ischemic preconditioning). Similarly, a 30 min exposure to the group I mGlu receptor agonist DHPG (10 microM) significantly reduced OGD neurotoxicity 24 h later (pharmacological preconditioning). Ischemic tolerance did not develop when either the selective mGlu1 antagonists LY367385 and 3-MATIDA or the AMPA/KA antagonist CNQX were present in the incubation medium during exposure to sublethal OGD. Neither the NMDA antagonist MK801 nor the mGlu5 antagonist MPEP affected the preconditioning process. On the other hand, pharmacological preconditioning was prevented not only by LY367385 or CNQX, but also by MPEP. In preconditioned slices, the toxic responses to AMPA or NMDA were reduced. The neurotoxicty of 100 microM DHPG in slices simultaneously exposed to a mild (20 min) OGD was differentially altered in the two preconditioning paradigms. After ischemic preconditioning, DHPG neurotoxicity was reduced in a manner that was sensitive to LY367385 but not to MPEP, whereas after pharmacological preconditioning it was enhanced in a manner that was sensitive to MPEP but not to LY367385. Our results show that mGlu1 and mGlu5 receptors are differentially involved in the induction and expression of ischemic tolerance following two diverse preconditioning stimuli.
机译：已经提出谷氨酸受体的激活是诱导缺血耐受的关键因素。我们使用暴露于30分钟氧-葡萄糖剥夺（OGD）的器官型大鼠海马切片来评估CA1子区域缺血后锥体细胞的死亡。在该模型中，在暴露于有毒的OGD前24小时暴露于OGD 10分钟没有致死性，并将随后的OGD神经毒性降低了约53％（缺血预处理）。同样，暴露于I组mGlu受体激动剂DHPG（10 microM）30分钟可显着降低24小时后的OGD神经毒性（药理预处理）。当暴露于亚致死性OGD期间，温育培养基中存在选择性mGlu1拮抗剂LY367385和3-MATIDA或AMPA / KA拮抗剂CNQX时，不会产生缺血耐受。 NMDA拮抗剂MK801和mGlu5拮抗剂MPEP均不影响预处理过程。另一方面，不仅可以通过LY367385或CNQX来预防药理预处理，还可以通过MPEP来预防。在预处理切片中，对AMPA或NMDA的毒性反应降低。同时暴露于轻度（20分钟）OGD的切片中100 microM DHPG的神经毒性在两种预处理范例中有所不同。缺血预处理后，DHPG神经毒性以对LY367385敏感但对MPEP不敏感的方式降低，而药理预处理后DHPG神经毒性以对MPEP敏感但对LY367385不敏感的方式增强。我们的结果表明，在两种不同的预处理刺激后，mGlu1和mGlu5受体差异参与缺血耐受的诱导和表达。

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