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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Involvement of nitric oxide in pioglitazone memory improvement in morphine-induced memory impaired mice
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Involvement of nitric oxide in pioglitazone memory improvement in morphine-induced memory impaired mice

机译：一氧化氮参与吗啡诱导的记忆障碍小鼠的吡格列酮记忆改善

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Introduction: Pioglitazone, a PPAR-γ agonist, which is clinically used in treating diabetic patients, has been recently reported to have crucial roles in improving cognition and memory performance. Since the mechanisms involved in the neuroprotective effect of pioglitazone are not entirely understood, the current study was designed to investigate the possible interaction of pioglitazone with morphine in memory-impaired mice and the probable role of nitric oxide (NO) in this effect. Materials and methods: All the experiments were performed in passive avoidance and Y-maze paradigms. To induce memory impairment, mice were administered morphine (1, 3 and 10 mg/kg, s.c.) immediately before the training trial. Pioglitazone (20, 40 and 80 mg/kg, p.o.) was gavaged 2 h prior to the training trial. Further, an NO synthase inhibitor, L-NAME (10 mg/kg, i.p.), or an inducible NO synthase inhibitor, aminoguanidine (100 mg/kg, i.p.) was administered 30 min before the training trial to determine the possible involvement of NO in the restorative effect of pioglitazone. Results: 1) Morphine dose dependently impaired the acquisition of spatial memory and passive avoidance task. 2) Treatment with pioglitazone significantly improved the memory performance in morphine-treated mice in both tests. 3) In the passive avoidance task, L-NAME, but not aminoguanidine, altered the effect of pioglitazone on morphine-induced memory impairment. 4) In Y-maze discrimination, the memory improving effect of pioglitazone was reversed by both NO synthase inhibitors, L-NAME and aminoguanidine. Discussion: Our results demonstrate that the pioglitazone improving effect on the morphine-induced impairment of memory acquisition is at least in part through the NO pathway. It is suggested that in short term spatial recognition memory, both inducible and constitutive NO synthases are involved, but in the long term fear memory, only the constitutive NO synthases indicated a prominent role in the anti-amnestic effect of pioglitazone on morphine-induced memory impairment.
机译：简介：吡格列酮是一种PPAR-γ激动剂，已在临床上用于治疗糖尿病患者，最近据报道在改善认知和记忆能力方面起着至关重要的作用。由于尚未完全了解吡格列酮对神经保护作用的机制，因此本研究旨在研究吡格列酮与吗啡在记忆障碍小鼠中的可能相互作用，以及一氧化氮（NO）可能在这种作用中的作用。材料和方法：所有实验均在被动回避和Y迷宫范式下进行。为了诱导记忆力受损，在训练试验之前，立即给小鼠服用吗啡（1、3和10 mg / kg，皮下注射）。在训练试验前2小时，对吡格列酮（20、40和80 mg / kg，口服）进行灌胃。此外，在训练试验前30分钟给药一氧化氮合酶抑制剂L-NAME（10 mg / kg，ip）或诱导型一氧化氮合酶抑制剂氨基胍（100 mg / kg，ip），以确定可能的一氧化氮参与在吡格列酮的修复作用中。结果：1）吗啡剂量依赖性地损害了空间记忆的获得和被动回避任务。 2）在两种测试中，吡格列酮治疗均显着提高了吗啡治疗小鼠的记忆力。 3）在被动回避任务中，L-NAME（而非氨基胍）改变了吡格列酮对吗啡诱导的记忆障碍的作用。 4）在Y-迷宫识别中，吡格列酮的记忆改善作用被NO合酶抑制剂L-NAME和氨基胍逆转。讨论：我们的结果表明吡格列酮对吗啡诱导的记忆获得性损伤的改善作用至少部分是通过NO途径实现的。建议在短期空间识别记忆中涉及诱导型和组成型NO合成酶，但在长期恐惧记忆中，仅组成型NO合成酶在吡格列酮对吗啡诱导的记忆的抗遗忘作用中起重要作用。损害。

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