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TAIL SUSPENSION DISRUPTS COGNITION FUNCTION AND DOWN-REGULATES LEARNING-RELATED PROTEIN EXPRESSION IN RAT HIPPOCAMPUS

机译:尾悬架扰乱了对大鼠海马的认知功能和下调学习相关的蛋白质表达

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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 MG F 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.
机译:目的:作为宇航员健康的挑战,微匍匐在一系列神经紊乱的病因中起着重要作用,例如空间运动疾病,空间适应综合征(SAS)和认知障碍。然而,这些生理效应的细节仍然不清楚。除神经元死亡之外,病情蛋白质似乎在这些过程中发挥作用。例如,已显示NMDA受体(NR)以影响神经元结构和突触可塑性。本研究旨在模拟微匍匐对认知函数和学习相关蛋白表达的影响。方法论:我们雇用7天尾悬架以模拟微匍匐,并研究了莫里斯水迷宫试验以及与蛋白质印迹试验的学习相关蛋白表达的空间记忆能力。结果:Sprague-Dawley(SD)大鼠的行为分析显示,空间学习受损。尾悬浮的大鼠表现出表达NR1 / 2B和CAMKII和CREB1的磷酸化,其被NR活化。另外,通过其下游NRF2介导的血红素氧合酶-1(HO-1)进行了机械生长因子(MGF)。与这些发现一致,海马的NR1 / 2B和MG F途径在模拟失重下显示出显着的缺陷。结论:在一起,这些数据支持NR和MGF的作用,作为模拟微观度诱导的认知变化中的调节剂,并提高内存相关蛋白质的可能性可能有助于模拟微蛋白下的认知障碍阵列。

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