a Department of Psychology, Northern Illinois University , DeKalb , IL , USA.
Stress. 2019 Sep;22(5):603-618. doi: 10.1080/10253890.2019.1617691. Epub 2019 May 28.
Previous research indicates that loneliness and social isolation may contribute to behavioral disorders and neurobiological dysfunction. Environmental enrichment (EE), including both cognitive and physical stimulation, may prevent some behavioral, endocrine, and cardiovascular consequences of social isolation; however, specific neural mechanisms for these benefits are still unclear. Therefore, this study examined potential neuroendocrine protective effects of both EE and exercise. Adult female prairie voles were randomly assigned to one of four experimental conditions: paired control, social isolation/sedentary, social isolation/EE, and social isolation/voluntary exercise. All isolated animals were housed individually for 8 weeks, while paired animals were housed with their respective sibling for 8 weeks. Animals in the EE and voluntary exercise conditions received EE items (including a running wheel) and a running wheel only, respectively, at week 4 of the isolation period. At the end of the experiment, plasma and brains were collected from all animals for corticosterone and FosB and delta FosB (FosB/ΔFosB) - immunoreactivity in stress-related brain regions. Overall, social isolation increased neuroendocrine stress responses, as reflected by the elevation of corticosterone levels and increased FosB/ΔFosB-immunoreactivity in the basolateral amygdala (BLA) compared to paired animals; EE and voluntary exercise attenuated these increases. EE and exercise also increased FosB/ΔFosB-immunoreactivity in the medial prefrontal cortex (mPFC) compared to other conditions. Limbic structures statistically mediated hypothalamic immunoreactivity in EE and exercise animals. This research has translational value for socially isolated individuals by informing our understanding of neural mechanisms underlying responses to social stressors. Highlights Prolonged social isolation increased basal corticosterone levels and basolateral amygdala immunoreactivity. Environmental enrichment and exercise buffered corticosterone elevations and basolateral amygdala hyperactivity. Protective effects of environmental enrichment and exercise may be mediated by medial prefrontal cortex and limbic structures.
先前的研究表明，孤独和社会隔离可能导致行为障碍和神经生物学功能障碍。环境丰富（EE），包括认知和身体刺激，可能预防社会隔离的一些行为、内分泌和心血管后果；然而，这些益处的具体神经机制仍不清楚。因此，本研究检查了 EE 和运动的潜在神经内分泌保护作用。成年雌性草原田鼠被随机分配到四个实验条件之一：配对对照组、社会隔离/久坐组、社会隔离/EE 组和社会隔离/自愿运动组。所有隔离动物均单独饲养 8 周，而配对动物则与其各自的兄弟姐妹一起饲养 8 周。在隔离期的第 4 周，EE 和自愿运动条件下的动物分别获得了 EE 物品（包括跑步轮）和仅跑步轮。实验结束时，从所有动物中收集血浆和大脑，用于检测应激相关脑区的皮质酮和 FosB 和 delta FosB（FosB/ΔFosB）免疫反应。总的来说，与配对动物相比，社会隔离会增加神经内分泌应激反应，表现为皮质酮水平升高和外侧杏仁核（BLA）中 FosB/ΔFosB 免疫反应增强；EE 和运动减轻了这些增加。与其他条件相比，EE 和运动还增加了内侧前额叶皮层（mPFC）中的 FosB/ΔFosB 免疫反应。边缘结构在 EE 和运动动物的下丘脑免疫反应中具有统计学意义。本研究通过告知我们对社交应激源反应的神经机制的理解，对社会隔离个体具有转化价值。要点 长期社会隔离增加了基础皮质酮水平和外侧杏仁核免疫反应。环境丰富和运动缓冲了皮质酮升高和外侧杏仁核活动过度。环境丰富和运动的保护作用可能通过内侧前额叶皮层和边缘结构介导。
