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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 >Kainic acid-induced changes in the opioidociceptin system and the stress/toxicity pathways in the rat hippocampus
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Kainic acid-induced changes in the opioidociceptin system and the stress/toxicity pathways in the rat hippocampus

机译：海藻酸诱导的大鼠海马阿片样物质/伤害感受器系统的变化以及应激/毒性途径

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Excitotoxicity is a contributing factor to the pathogenesis of acute or chronic neurodegenerative disease states. Kainic acid (KA) is an excitotoxic substance and the administration of it to rodents induces seizure activity (status epilepticus, SE) and leads to neurodegeneration. In this study the effect of KA-induced excitotoxicity on the G-protein activations and the gene expression levels of the opioidociceptin system receptors as MOPr, KOPr, DOPr, ORL-1, and PNOC (N/OFQ) were investigated, and the regulator effect of naloxone (Nal) on the gene expressions of the opioid system receptors against KA-induced seizures in the rat hippocampus was tested. In addition, the expression levels of stress-toxicity genes were assessed in the hippocampus following KA-induced excitotoxicity in order to determine the potential genetic targets which can be helpful for neuroprotective interventions. Our results indicate that the KA-induced excitotoxicity increased the mRNA levels of MOPr, DOPr, KOPr, PNOC, and ORL-1. However, G-protein activations of MOPr, DOPr, and KOPr remained relatively unchanged while both the potency and efficacy of N/OFQ were significantly increased. The PCR array data showed that KA-induced excitotoxicity altered the expression levels of genes in the cellular stress or toxicity pathways. Our data suggests that the induction of the opioidociceptin system may be involved in the cellular stress response following a neurodegenerative insult and that the genes modulated by the KA-treatment in the stress-toxicity pathways may be evaluated as targets of potential neuroprotective interventions.
机译：兴奋性毒性是急性或慢性神经退行性疾病状态的发病机理的促成因素。海藻酸（KA）是一种兴奋性毒性物质，将其施用给啮齿动物会引起癫痫发作（癫痫持续状态，SE）并导致神经退行性变。在这项研究中，KA引起的兴奋性毒性对G蛋白活化和阿片样物质/伤害感受素系统受体MOPr，KOPr，DOPr，ORL-1和PNOC（N / OFQ）的基因表达水平的影响，以及测试了纳洛酮（Nal）对阿片样物质受体在大鼠海马中抗KA诱发的癫痫发作的调节作用。另外，在KA诱导的兴奋性毒性之后评估海马中的应激毒性基因的表达水平，以确定可能有助于神经保护性干预的潜在遗传靶标。我们的结果表明，KA诱导的兴奋性毒性增加了MOPr，DOPr，KOPr，PNOC和ORL-1的mRNA水平。但是，MOPr，DOPr和KOPr的G蛋白活化相对保持不变，而N / OFQ的效力和功效均显着提高。 PCR阵列数据显示，KA诱导的兴奋性毒性改变了细胞应激或毒性途径中基因的表达水平。我们的数据表明，在神经退行性损伤后，阿片样物质/ nociceptin系统的诱导可能参与细胞应激反应，并且在应激毒性途径中由KA处理调节的基因可能被评估为潜在的神经保护性干预措施的靶标。

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