Stress injuries and autophagy in mouse hippocampus after chronic cold exposure

• Main Authors: Ting-ting Qu, Jie-xin Deng, Rui-ling Li, Zhan-jun Cui, Xiao-qing Wang, Lai Wang, Jin-bo Deng
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2017-01-01
• Series: Neural Regeneration Research
• Subjects: nerve regeneration; chronic cold exposure; oxidative stress; autophagy; microglial cells; neuroimmunoreactivity; hippocampal CA1 area; estrogen; neural regeneration
• Online Access: http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=3;spage=440;epage=446;aulast=Qu

Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases. Estrogen might participate in neuroprotection after cold exposure, but its precise mechanism remains unclear. In this study, mice were exposed to 10°C for 7 days and 0–4°C for 30 days to induce a model of chronic cold exposure. Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions, MAP1LC3-labeled autophagic cells, Iba1-labeled activated microglia, and interleukin-1β-positive pyramidal cells were increased in the hippocampal CA1 area. Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor, G protein-coupled receptor 30. These results indicate that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations, including oxidative stress, neuronal autophagy, and neuroimmunoreactivity. Moreover, estrogen exerts a neuroprotective effect on cold exposure.