Furuhashi Tsubasa, Sakamoto Kazuichi
Graduate School of Life and Environmental Sciences, University of Tsukuba, Japan.
Graduate School of Life and Environmental Sciences, University of Tsukuba, Japan.
Physiol Behav. 2017 Jan 1;168:20-23. doi: 10.1016/j.physbeh.2016.10.012. Epub 2016 Oct 18.
Autonomic nervous system (ANS) imbalances are involved in the etiology of cancer, allergy, and collagen diseases. Previously, we hypothesized that FoxO and HSF-1 limit autonomic stress responses via negative feedback on the ANS. Here, we evaluated the role of AKT, a negative regulator of FoxO, during activation of the ANS by loneliness stress in mice. Spontaneous motility was increased during loneliness stress and decreased after release from stress. The AKT activator SC79 attenuated stress-induced spontaneous motility, whereas the AKT inhibitor API-2 prevented decreases in motility after stress release. Our results show that AKT activity regulates ANS responses to loneliness stress.
自主神经系统（ANS）失衡与癌症、过敏和胶原疾病的病因有关。此前，我们假设FoxO和HSF-1通过对自主神经系统的负反馈来限制自主应激反应。在此，我们评估了FoxO的负调节因子AKT在小鼠孤独应激激活自主神经系统过程中的作用。孤独应激期间自发运动增加，应激解除后减少。AKT激活剂SC79减弱了应激诱导的自发运动，而AKT抑制剂API-2则阻止了应激解除后运动能力的下降。我们的结果表明，AKT活性调节自主神经系统对孤独应激的反应。
