Negative rebound in hippocampal neurogenesis following exercise cessation
Negative rebound in hippocampal neurogenesis following exercise cessation
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DOI：
10.1152/ajpregu.00397.2016
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发表时间：
2017-03-01
影响因子：
2.8
通讯作者：
Kita, Ichiro
中科院分区：
文献类型：
--
作者：
Nishijima, Takeshi;Kamidozono, Yoshika;Kita, Ichiro
体育锻炼可以改善大脑功能，但运动停止的影响在很大程度上是未知的。本研究探讨了运动停止后海马神经发生的时间过程。将雄性C57 BL/6小鼠随机分配到对照组（Con）或运动停止组（ExC）。ExC组小鼠在带有转轮的笼子中饲养8周，随后置于标准笼子中停止运动。运动导致齿状回中双皮质素（DCX）阳性未成熟神经元的密度显著增加（第0周）。运动停止后，DCX阳性神经元的密度逐渐下降，并在停止后5和8周显着低于Con组，表明运动停止导致海马神经发生的负性反弹。免疫组织化学分析表明，神经发生的负反弹是由细胞存活减少引起的，而不是由细胞增殖和神经成熟的抑制引起的。无论是Delta FosB，参与神经发生调节的转录因子的表达升高，也没有增加血浆皮质酮，参与负性神经发生反弹。重要的是，运动停止抑制步行活动，活动和DCX阳性神经元密度的变化之间的显着相关性表明，活动减少参与神经发生障碍。运动停止后强迫跑台跑步不能防止负性神经发生反弹。这项研究表明，停止运动或减少体力活动与海马功能受损的风险增加有关，这可能会增加对压力诱导的情绪障碍的脆弱性。
Physical exercise can improve brain function, but the effects of exercise cessation are largely unknown. This study examined the time-course profile of hippocampal neurogenesis following exercise cessation. Male C57BL/6 mice were randomly assigned to either a control (Con) or an exercise cessation (ExC) group. Mice in the ExC group were reared in a cage with a running wheel for 8 wk and subsequently placed in a standard cage to cease the exercise. Exercise resulted in a significant increase in the density of doublecortin (DCX)-positive immature neurons in the dentate gyrus (at week 0). Following exercise cessation, the density of DCX-positive neurons gradually decreased and was significantly lower than that in the Con group at 5 and 8 wk after cessation, indicating that exercise cessation leads to a negative rebound in hippocampal neurogenesis. Immunohistochemistry analysis suggests that the negative rebound in neurogenesis is caused by diminished cell survival, not by suppression of cell proliferation and neural maturation. Neither elevated expression of Delta FosB, a transcription factor involved in neurogenesis regulation, nor increased plasma corticosterone, were involved in the negative neurogenesis rebound. Importantly, exercise cessation suppressed ambulatory activity, and a significant correlation between change in activity and DCX-positive neuron density suggested that the decrease in activity is involved in neurogenesis impairment. Forced treadmill running following exercise cessation failed to prevent the negative neurogenesis rebound. This study indicates that cessation of exercise or a decrease in physical activity is associated with an increased risk for impaired hippocampal function, which might increase vulnerability to stress-induced mood disorders.