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Abstract：
UNASSIGNED: The ovariectomized (OVX) rodent model is most widely used for studying the influence of estrogen deprivation on memory. However, the results of these studies are inconsistent, in that the memory of OVX rodents shows either impairment or no change. These inconsistent outcomes increase the difficulty of researching neurochemical mechanisms and evaluating drug efficacy. One possible explanation for these discrepancies might be that the time point for memory examination after OVX varies considerably among studies. The aim of our study was to investigate the effects of estrogen deprivation on memory and the expression of memory-related proteins at different times after OVX.
UNASSIGNED: Novel object recognition (NOR), step-through passive avoidance (STPA) and the Morris water maze (MWM) were performed to evaluate the memory performance of mice at different times after OVX. The expressions of BDNF, TrkB, ULK1 and LC3II/LC3I in the hippocampus were also assessed to explore the relevant mechanisms.
UNASSIGNED: After OVX, a significant memory impairment was found in the STPA test at 4 weeks. In the NOR and MWM tests, however, memory deficits were not observed until 8 weeks post-OVX. Interestingly, at 8 weeks, a memory rebound was found in the STPA test. In the hippocampus, the levels of BDNF and TrkB in OVX mice were markedly decreased at 4 and 8 weeks. Subsequently, a significant decrease in the ULK1 and LC3II/LC3I level in OVX mice was observed at 8 weeks.
UNASSIGNED: Memory impairment in mice was observed as early as 4 weeks after OVX, although there was a possibility of memory rebound with the prolongation of estrogen deprivation. Eight weeks of estrogen deprivation would be more likely to induce hippocampus-dependent memory impairment. This progressive impairment of memory might be due to the downregulation of the BDNF/TrkB signaling pathway at the early post-OVX stage, while the decrease of autophagy level in the later stage might also contribute to these progressive alterations. The underlying relationship between the BDNF/TrkB signaling pathway and autophagy in this progressive impairment of memory requires further study.
UNASSIGNED: Novel object recognition (NOR), step-through passive avoidance (STPA) and the Morris water maze (MWM) were performed to evaluate the memory performance of mice at different times after OVX. The expressions of BDNF, TrkB, ULK1 and LC3II/LC3I in the hippocampus were also assessed to explore the relevant mechanisms.
UNASSIGNED: After OVX, a significant memory impairment was found in the STPA test at 4 weeks. In the NOR and MWM tests, however, memory deficits were not observed until 8 weeks post-OVX. Interestingly, at 8 weeks, a memory rebound was found in the STPA test. In the hippocampus, the levels of BDNF and TrkB in OVX mice were markedly decreased at 4 and 8 weeks. Subsequently, a significant decrease in the ULK1 and LC3II/LC3I level in OVX mice was observed at 8 weeks.
UNASSIGNED: Memory impairment in mice was observed as early as 4 weeks after OVX, although there was a possibility of memory rebound with the prolongation of estrogen deprivation. Eight weeks of estrogen deprivation would be more likely to induce hippocampus-dependent memory impairment. This progressive impairment of memory might be due to the downregulation of the BDNF/TrkB signaling pathway at the early post-OVX stage, while the decrease of autophagy level in the later stage might also contribute to these progressive alterations. The underlying relationship between the BDNF/TrkB signaling pathway and autophagy in this progressive impairment of memory requires further study.
摘要：
■去卵巢（OVX）啮齿动物模型最广泛地用于研究雌激素剥夺对记忆的影响。然而,这些研究的结果是不一致的，OVX啮齿动物的记忆显示损伤或无变化。这些不一致的结果增加了研究神经化学机制和评估药物疗效的难度。这些差异的一种可能的解释可能是OVX后记忆检查的时间点在研究中差异很大。我们研究的目的是研究雌激素剥夺对OVX后不同时间记忆和记忆相关蛋白表达的影响。
■新型物体识别(NOR)，进行逐步被动回避（STPA）和Morris水迷宫（MWM）以评估OVX后不同时间小鼠的记忆表现。BDNF的表达，TrkB,还评估了海马中的ULK1和LC3II/LC3I以探索相关机制。
■在OVX之后，在4周时的STPA测试中发现了显著的记忆障碍.在NOR和MWM测试中，然而,直到OVX后8周才观察到记忆障碍.有趣的是,在8周的时候,在STPA测试中发现记忆反弹。在海马中,OVX小鼠的BDNF和TrkB水平在4周和8周时显著降低。随后，在8周时观察到OVX小鼠ULK1和LC3II/LC3I水平显著下降.
■早在OVX后4周就观察到小鼠记忆障碍，尽管随着雌激素剥夺的延长，记忆可能会反弹。八周的雌激素剥夺更有可能诱发海马依赖性记忆障碍。这种记忆的进行性损害可能是由于在OVX后早期BDNF/TrkB信号通路的下调，而后期自噬水平的降低也可能导致这些进行性改变。BDNF/TrkB信号通路与自噬在这种进行性记忆损伤中的潜在关系需要进一步研究。
■新型物体识别(NOR)，进行逐步被动回避（STPA）和Morris水迷宫（MWM）以评估OVX后不同时间小鼠的记忆表现。BDNF的表达，TrkB,还评估了海马中的ULK1和LC3II/LC3I以探索相关机制。
■在OVX之后，在4周时的STPA测试中发现了显著的记忆障碍.在NOR和MWM测试中，然而,直到OVX后8周才观察到记忆障碍.有趣的是,在8周的时候,在STPA测试中发现记忆反弹。在海马中,OVX小鼠的BDNF和TrkB水平在4周和8周时显著降低。随后，在8周时观察到OVX小鼠ULK1和LC3II/LC3I水平显著下降.
■早在OVX后4周就观察到小鼠记忆障碍，尽管随着雌激素剥夺的延长，记忆可能会反弹。八周的雌激素剥夺更有可能诱发海马依赖性记忆障碍。这种记忆的进行性损害可能是由于在OVX后早期BDNF/TrkB信号通路的下调，而后期自噬水平的降低也可能导致这些进行性改变。BDNF/TrkB信号通路与自噬在这种进行性记忆损伤中的潜在关系需要进一步研究。
