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首页> 外文会议>International astronautical congress >TAIL SUSPENSION DISRUPTS COGNITION FUNCTION AND DOWN-REGULATES LEARNING-RELATED PROTEIN EXPRESSION IN RAT HIPPOCAMPUS
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TAIL SUSPENSION DISRUPTS COGNITION FUNCTION AND DOWN-REGULATES LEARNING-RELATED PROTEIN EXPRESSION IN RAT HIPPOCAMPUS

机译：尾部悬浮破坏大鼠海马的认知功能并下调与学习相关的蛋白表达

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Purpose: As a challenge to astronauts' health, microgravity plays an important role in the etiology of a series of neurological disturbances such as space motion sickness, space adaptation syndrome (SAS) and cognitive disorders. Yet the details of these physiological effects remain unclear. In addition to neuron death, incellular proteins appear to play a role in these processes. For instance, NMDA receptor (NR) has been shown to affect neuronal structure and synaptic plasticity. The present study is aimed at the effects of simulated microgravity on cognition function and learning-related protein expression. Methodology: We employed 7 days tail-suspension to simulate microgravity and investigated the spatial memory capability with Morris water maze test as well as the learning-related protein expression with Western Blotting test. Results: Behavioral analysis of Sprague-Dawley (SD) rats revealed that spatial learning was impaired. Tail-suspended rats exhibited decrease in the expression NR1/2B and phosphorylation of CaMKII and CREB1, which were activated by NR. Additionally, mechano-growth factor (MGF) was downregulated with its downstream Nrf2 mediated neuroprotection of heme oxygenase-1 (HO-1). Consistent with these findings, NR1/2B and MGF pathway in hippocampus displayed significant deficits under simulated weightlessness. Conclusions: Together, these data support a role of NR and MGF as regulator in cognitive change induced by simulated-microgravity and raise the possibility the dysregulation of memory-related protein may contribute to an array of cognitive disorders under simulated-microgravity. Keywords: Microgravity, Spatial learning, NMDA receptor, Mechano-growth factor Acknowledgments This study was supported by the National Natural Science Foundation of China (Grant No. 30973686), Medicinal Science and Techology Research Project (Grant No. BWS11J052), the National Science and Techology Major Project (Grant No. 2012ZX09J12201) and the Foundation of State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center (Grant No. SMFA09A06, SMFA10B01, SMFA12B05).
机译：目的：作为对宇航员健康的挑战，微重力在一系列神经系统疾病的病因中起着重要作用，例如空间晕动症，空间适应综合症（SAS）和认知障碍。这些生理作用的细节仍不清楚。除神经元死亡外，细胞内蛋白似乎在这些过程中也起作用。例如，已显示NMDA受体（NR）影响神经元结构和突触可塑性。本研究旨在模拟微重力对认知功能和学习相关蛋白表达的影响。方法：我们使用7天的尾部悬架来模拟微重力，并通过Morris水迷宫测试研究了空间记忆能力，并通过Western Blotting测试研究了与学习有关的蛋白质表达。结果：对Sprague-Dawley（SD）大鼠的行为分析表明，空间学习受到损害。尾部悬吊的大鼠表现出NR1 / 2B的表达减少，以及被NR激活的CaMKII和CREB1的磷酸化。此外，机械生长因子（MGF）被其下游Nrf2介导的血红素加氧酶-1（HO-1）的神经保护作用下调。与这些发现一致的是，在模拟失重条件下，海马中的NR1 / 2B和MGF途径表现出明显的缺陷。结论：这些数据共同支持了NR和MGF作为模拟微重力所致认知变化的调节剂，并增加了记忆相关蛋白失调可能导致一系列模拟微重力下的认知障碍的可能性。关键词：微重力;空间学习; NMDA受体;机械生长因子致谢：这项研究得到了中国国家自然科学基金（批准号30973686），药物科学与技术研究项目（批准号BWS11J052），国家科学的支持。科技重大专项（批准号：2012ZX09J12201）和中国航天研究与培训中心航天医学基础与应用国家重点实验室基金（批准号：SMFA09A06，SMFA10B01，SMFA12B05）。

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