Venezia A C, Quinlan E, Roth S M
Department of Exercise Science and Sport, The University of Scranton, Scranton, PA, USA.
Department of Kinesiology, School of Public Health, University of Maryland, College Park, MD, USA.
Genes Brain Behav. 2017 Nov;16(8):800-811. doi: 10.1111/gbb.12394. Epub 2017 Jun 22.
Research in human subjects suggests that acute exercise can improve memory performance, but the qualities of the exercise necessary to promote improved memory, and the signaling pathways that mediate these effects are unknown. Brain-derived neurotrophic factor (Bdnf), noradrenergic signaling, and post-translational modifications to AMPA receptors have all been implicated in the enhancement of memory following emotional or physical arousal; however, it is not known if a single bout of exercise is sufficient to engage these pathways. Here we use a rodent model to investigate the effects of acute and chronic exercise on hippocampal transcript-specific Bdnf expression and phosphorylation of the GluR1 subunit of the AMPA-type glutamate receptor. A single bout of treadmill exercise was insufficient to mimic the increased expression of GluR1 protein and phosphorylation at Ser845 observed following 1 month of voluntary wheel running. However, acute exercise was sufficient to increase Bdnf transcript IV messenger RNA (mRNA) expression in sedentary subjects, but not subjects housed for 1 month with a running wheel. High-intensity acute exercise increased total Bdnf mRNA in sedentary mice, but not above levels observed following chronic access to the running wheel. Although depletion of central noradrenergic signaling with DSP-4 reduced Bdnf IV mRNA, the effect of acute exercise on Bdnf mRNA persisted. Our characterization of the effects of acute exercise on Bdnf expression and persistence in the absence of noradrenergic modulation may inform strategies to employ physical activity to combat cognitive aging and mental health disorders.
对人类受试者的研究表明，急性运动可以改善记忆表现，但促进记忆改善所需的运动特质以及介导这些效应的信号通路尚不清楚。脑源性神经营养因子（Bdnf）、去甲肾上腺素能信号传导以及对AMPA受体的翻译后修饰都与情绪或身体兴奋后记忆的增强有关；然而，单次运动是否足以激活这些通路尚不清楚。在这里，我们使用啮齿动物模型来研究急性和慢性运动对海马体转录本特异性Bdnf表达以及AMPA型谷氨酸受体GluR1亚基磷酸化的影响。单次跑步机运动不足以模拟在自愿轮转1个月后观察到的GluR1蛋白表达增加和Ser845位点的磷酸化。然而，急性运动足以增加久坐不动的受试者中Bdnf转录本IV信使核糖核酸（mRNA）的表达，但对于在有转轮的环境中饲养1个月的受试者则不然。高强度急性运动增加了久坐不动小鼠的总Bdnf mRNA，但未超过长期使用转轮后观察到的水平。尽管用DSP-4耗尽中枢去甲肾上腺素能信号传导会降低Bdnf IV mRNA，但急性运动对Bdnf mRNA的影响仍然存在。我们对急性运动在去甲肾上腺素能调节缺失情况下对Bdnf表达和持续性影响的表征，可能为采用体育活动来对抗认知衰老和心理健康障碍的策略提供信息。
