Social isolation increased ADAR1 expressions leading to cognitive deficits of miceWei Chen, Dong An, Hong Xu, Xiaoxin Cheng, Shiwei Wang, Weizhi Yu, Deqin Yu, Dan Zhao, Yiping Sun, Wuguo Deng, Yiyuan Tang, Shengming Yin A lot of literature show that social isolation stress could be a key reason that leads to cognitive deficits for both humans and rodent models; however, the detailed mechanisms are still not clear completely. ADAR1 (Adenosine deaminase acting on RNA) is an enzyme involved in RNA editing that has a close relation to cognitive function. We hypothesize that social isolation stress may impact the expression of ADAR1, leading to cognitive deficits.To prove our hypothesis, we evaluated the cognition ability of the mice isolated for different durations (2, 4, and 8 weeks) using object recognition and object location tests;we also measured ADAR1 expressions in hippocampus and cortex using immunohistochemistry and western blot. Our study showed that social isolation stress significantly induced spatial and non-spatial cognition deficits. In addition, social isolation significantly increased both the immuno reactivity and protein expressions of ADAR1 in the hippocampus and frontal cortex. Furthermore, we found that adolescent re-socialization recovered not only the cognition deficits but also the increased ADAR1 protein expression in hippocampus and the increased number of ADAR1 positive cells in frontal cortex of the isolated mice. In conclusion, social isolation stress significantly increased ADAR1 expressions in the hippocampus and cortex, leading to cognitive deficits. A lot of literatures show that social isolation stress could be a key reason that leads to cognitive deficits for both humans and rodent models; however, the detailed mechanisms are still not clear completely. ADAR1 (Adenosine deaminase acting on RNA) is an enzyme involved in RNA editing that has a close relation to cognitive function. We hypothesize that social isolation stress may impact the expression of ADAR1, leading to cognitive deficits. To prove our hypothesis, we evaluated the cognition ability of the mice isolated for different durations (2, 4, and 8 weeks) using object recognition and object location tests; we also measured ADAR1 expressions in hippocampus and cortex using immunohistochemistry and western blot. Our study showed that social isolation stress significantly induced spatial and non-spatial cognition deficits. In addition, social isolation significantly increased both the immunoreactivity and protein expressions of ADAR1 in the hippocampus and frontal cortex.Furthermore, we found that adolescent re-socialization recovered not only the cognition deficits but also the increased ADAR1 protein expression in hippocampus and the increased number of ADAR1 positive cells in frontal cortex of the isolated mice. In conclusion, social isolation stress significantly increased ADAR1 expressions in the hippocampus and cortex, leading to cognitive deficits.Key words: social isolation; cognitive ability; ADAR1 Social isolation is a...
Altered ADAR1 in mice affected by social isolation stressinduced cognitive deficitsAdenosine deaminase acting on RNA (ADAR) activity increases in response to inflammation. Social isolation stress is related to neuroinflammation; however, it remains unclear whether ADAR1 is altered in response to social isolation stress-induced cognitive deficits. To investigate our hypothesis that ADAR1 displayed patterns of change in response to social isolation stress, we addressed this issue systemically by isolating Kunming mice for 2, 4 and 8 weeks individually since postnatal 21 days to set up isolation mouse model. Furthermore, we arranged re-socialization group to evaluate the alterations of ADAR1 in the cognitive deficits recovery. The results of behavior tests showed that social isolation stress resulted in cognitive dysfunction, which was recovered by resocialization in re-gregarious rearing group. Furthermore, the immunohistochemistry and western blot results displayed that both the immunoreactivity and protein expression of ADAR1 in the hippocampus and frontal cortex increased obviously as compared to the same age mice without isolation. The above abnormal alterations of ADAR1 were recovered by re-socialization in re-gregarious rearing group. Our study supports the hypothesis that ADAR1 is altered in mice affected by social isolation stress-induced Social isolation stress is related to neuroinflammation; however, it remains unclear whether ADAR1 alters in response to social isolation stress-induced cognitive deficits. To investigate our hypothesis that ADAR1 displayed patterns of change in response to social isolation stress, we addressed this issue systemically by isolating Kunming mice for 2, 4 and 8 weeks individually since postnatal 21 days to set up isolation mouse model. Furthermore, we arranged re-socialization group to evaluate the alterations of ADAR1 in the cognitive deficits recovery. The results of behavior tests showed that social isolation stress resulted in cognitive dysfunction, which was recovered by re-socialization in re-gregarious rearing group. Furthermore, the immunohistochemistry and western blot results displayed that both the immunoreactivity and protein expression of ADAR1 in the hippocampus and frontal cortex increased obviously as compared to the same age mice without isolation. The above abnormal alterations of ADAR1 were recovered by re-socialization in re-gregarious rearing group. Our study supports the hypothesis that ADAR1 is altered in the social isolation stress-induced cognitive deficits.
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