Institute of Theoretical and Experimental Biophysics, RAS, Pushchino, Russia, 142290.
Pushchino State Institute of Natural Sciences, Pushchino, Russia.
J Mol Neurosci. 2019 Feb;67(2):258-264. doi: 10.1007/s12031-018-1233-9. Epub 2018 Nov 30.
A variety of localization and signaling properties of eight subtypes of metabotropic glutamate receptors (mGluRs) in the brain provide glutamate an important regulatory role in many processes, including neurodegeneration and repair of neuronal damage. To identify specific subtypes of mGluRs, which are involved in neurodegeneration process, we assessed expression levels of their genes under pathophysiological conditions. Using quantitative real-time RT-PCR analysis, we studied transcription levels of mGlu2-5 and mGlu7 genes in the hippocampus after its damage by neurotoxicant trimethyltin chloride (TMT) in Wistar rats. This organotin compound is known to cause neurodegeneration in the brain, especially in the hippocampus. Morphological studies confirmed neuronal damage in CA3-CA4 subfields of the hippocampus 6 weeks after the treatment with TMT. Step-through passive avoidance test revealed memory deterioration in rat-treated TMT. Interestingly, 3 and 6 weeks after the treatment with TMT, expression levels of the mGlu2 and mGlu7 genes were not changed in comparison to the control values while expression level of mGlu4 genes was upregulated throughout the whole studied period of TMT action. The dynamics of mGlu3 gene expression revealed the existence of neuroinflammation 3 weeks after the treatment with TMT, which was further confirmed by the upregulation of cyclooxygenase-2 gene expression. The expression level of mGlu5 receptors was downregulated 6 weeks after the treatment with TMT. Our results revealed a significant role of mGlu4, mGlu5, and mGlu3 receptors in the neurodegenerative/reparative processes in the hippocampus after the treatment with TMT. Ligands of these receptor subtypes can be, therefore, considered potential therapeutic targets for prevention or reduction of neurodegeneration.
八种代谢型谷氨酸受体 (mGluR) 亚型在大脑中的各种定位和信号转导特性赋予谷氨酸在许多过程中重要的调节作用,包括神经退行性变和神经元损伤的修复。为了确定参与神经退行性变过程的特定 mGluR 亚型,我们在病理生理条件下评估了它们的基因表达水平。使用定量实时 RT-PCR 分析,我们研究了 Wistar 大鼠神经毒性三甲基锡氯化物 (TMT) 损伤后海马中 mGlu2-5 和 mGlu7 基因的转录水平。这种有机锡化合物已知会导致大脑,特别是海马体的神经退行性变。形态学研究证实了 TMT 治疗后 6 周海马 CA3-CA4 亚区的神经元损伤。穿梭式被动回避测试显示 TMT 处理大鼠的记忆功能下降。有趣的是,与对照值相比,TMT 处理后 3 和 6 周,mGlu2 和 mGlu7 基因的表达水平没有变化,而 mGlu4 基因的表达水平在整个 TMT 作用研究期间均上调。mGlu3 基因表达的动态变化揭示了 TMT 治疗后 3 周存在神经炎症,这进一步通过环氧合酶-2 基因表达的上调得到证实。mGlu5 受体的表达水平在 TMT 处理后 6 周下调。我们的研究结果表明,在 TMT 处理后,海马体中 mGlu4、mGlu5 和 mGlu3 受体在神经退行性变/修复过程中发挥重要作用。因此,这些受体亚型的配体可以被认为是预防或减少神经退行性变的潜在治疗靶点。