Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.
Mol Cell Neurosci. 2013 Sep;56:375-83. doi: 10.1016/j.mcn.2013.07.011. Epub 2013 Jul 30.
Evidence suggests that regular exercise can protect against learning and memory impairment in the presence of insults such as sleep deprivation. The dentate gyrus (DG) area of the hippocampus is a key staging area for learning and memory processes and is particularly sensitive to sleep deprivation. The purpose of this study was to determine the effect of regular exercise on early-phase long-term potentiation (E-LTP) and its signaling cascade in the presence of sleep deprivation.
Rats were exposed to 4 weeks of regular treadmill exercise then subsequently sleep-deprived for 24h using the modified multiple platform model before experimentation. We tested the effects of exercise and/or sleep deprivation using electrophysiological recording in the DG to measure synaptic plasticity; and Western blot analysis to quantify the levels of key signaling proteins related to E-LTP.
Regular exercise prevented the sleep deprivation-induced impairment of E-LTP in the DG area as well as the sleep deprivation-associated decrease in basal protein levels of phosphorylated and total α calcium/calmodulin-dependent protein kinase II (P/total-CaMKII) and brain-derived neurotrophic factor (BDNF). High frequency stimulation (HFS) to the DG area was used to model learning stimuli and increased the P-CaMKII and BDNF levels in normal animals: yet failed to change these levels in sleep-deprived rats. However, HFS in control and sleep-deprived rats increased the levels of the phosphatase calcineurin. In contrast, exercise increased BDNF and P-CaMKII levels in exercised/sleep-deprived rats.
Regular exercise appears to exert a protective effect against sleep deprivation-induced spatial memory impairment by inducing hippocampal signaling cascades that positively modulate basal and stimulated levels of key effectors such as P-CaMKII and BDNF, while attenuating increases in the protein phosphatase calcineurin.
有证据表明，有规律的运动可以预防学习和记忆损伤，即使存在睡眠剥夺等损伤。海马齿状回（DG）区是学习和记忆过程的关键分期区，对睡眠剥夺特别敏感。本研究的目的是确定有规律的运动对睡眠剥夺时早期长时程增强（E-LTP）及其信号级联的影响。
大鼠接受 4 周的常规跑步机运动，然后使用改良的多平台模型进行 24 小时睡眠剥夺，然后进行实验。我们使用 DG 中的电生理记录测试运动和/或睡眠剥夺的影响，以测量突触可塑性；并使用 Western blot 分析来量化与 E-LTP 相关的关键信号蛋白的水平。
有规律的运动可预防睡眠剥夺引起的 DG 区 E-LTP 损伤，以及睡眠剥夺引起的磷酸化和总 α 钙/钙调蛋白依赖性蛋白激酶 II（P/total-CaMKII）和脑源性神经营养因子（BDNF）的基础蛋白水平下降。DG 区的高频刺激（HFS）用于模拟学习刺激，增加了正常动物的 P-CaMKII 和 BDNF 水平：但未能改变睡眠剥夺大鼠的这些水平。然而，HFS 增加了对照组和睡眠剥夺组大鼠的磷酸酶钙调神经磷酸酶的水平。相比之下，运动增加了运动/睡眠剥夺大鼠中 BDNF 和 P-CaMKII 的水平。
有规律的运动似乎通过诱导海马信号级联，对睡眠剥夺引起的空间记忆损伤产生保护作用，该信号级联正向调节关键效应物如 P-CaMKII 和 BDNF 的基础和刺激水平，同时减弱钙调神经磷酸酶的蛋白水平增加。
