ABSTRACT

Objectives: To investigate the effect on vascular dementia of involuntary exercise induced by functional electrical stimulation and of forced and voluntary exercise, focusing on the recovery of cognitive function and using a rat model of dementia.

Methods: A demential model was created in Wistar rats who were then given forced exercise, allowed voluntary exercise (wheel running) or had exercise induced through functional electrical stimulation. Their responses were quantified using a Morris water maze and by measuring long-term potentiation in the hippocampus. Immunohistochemical staining was used to evaluate neurogenesis in the hippocampus and Nissl staining was applied to visualize viable neuron loss in the DG sector. In addition, the levels of NMDAR1, AMPAR1, pAMPAR1, pCaMKII, CaMKII, Bcl-2 and Bax in the hippocampus were assessed by western blotting.

Results: All of the exercise groups showed a recovery of cognitive performance and improved long-term potentiation. The three modes of exercise all increased the number of DCX immunopositive cells and reduced losses of intact-appearing neurons in the hippocampal DG zones roughly equally. All proved about equally effective in increasing the levels of NMDAR1, pAMPAR1 and pCaMKII and increasing the Bcl-2/Bax ratio to protect neurons from apoptosis.

Conclusion: Exercise induced by electrical stimulation has beneficial effects comparable to those of other types of exercise for alleviating the cognitive deficits of vascular dementia.

摘要

目的：研究功能性电刺激诱导的不自主运动和强迫和自主运动对血管性痴呆的影响，重点关注认知功能的恢复，并使用痴呆大鼠模型。

方法：在 Wistar 大鼠中创建痴呆模型，然后对这些大鼠进行强制运动、允许自愿运动（轮跑）或通过功能性电刺激诱导运动。他们的反应是使用莫里斯水迷宫和测量海马体的长期增强来量化的。免疫组织化学染色用于评估海马中的神经发生，尼氏染色用于可视化 DG 部门中可行的神经元损失。此外，通过蛋白质印迹评估海马中 NMDAR1、AMPAR1、pAMPAR1、pCaMKII、CaMKII、Bcl-2 和 Bax 的水平。

结果：所有运动组均表现出认知能力的恢复和长期增强能力的改善。三种运动方式都增加了 DCX 免疫阳性细胞的数量，并大致相等地减少了海马 DG 区中完整出现的神经元的损失。所有这些都证明在增加 NMDAR1、pAMPAR1 和 pCaMKII 的水平以及增加 Bcl-2/Bax 比率以保护神经元免于细胞凋亡方面同样有效。

结论：电刺激诱发的运动对于缓解血管性痴呆的认知缺陷具有与其他运动类型相当的有益效果。