Liu Bingjin, Wang Lin, Cao Yun, Xu Weiqi, Shi Fangxiao, Tian Qing, Zhou Xinwen
Key Laboratory of Neurological Diseases of Education Ministry, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
Key Laboratory of Neurological Diseases of Education Ministry, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
Brain Res. 2017 Oct 1;1672:18-28. doi: 10.1016/j.brainres.2017.07.008. Epub 2017 Jul 17.
Posttraumatic hypothermia attenuates cognitive deficits caused by TBI when it is administered at an early stage. However, little is known regarding the effect of hypothermia pretreatment on cognitive deficits one month after TBI. In the current study, the behavior test revealed that hypothermia pretreatment mitigates the learning and memory impairment induced by TBI in mice. Hypothermia treatment significantly increased the expression of PSD93, PSD95 and NR2B one month after TBI in the cortex and hippocampus compared with the normothermia group. Hypothermia pretreatment also restored the decreased spine number and the impairment in LTP and decreased the number of activated microglia one month after TBI. On the other hand, hypothermia pretreatment increased glucose metabolism in TBI mice. Taken together, these data suggested that hypothermia pretreatment is an effective method with which to prevent spine loss, maintain normal LTP and preserve learning and memory function after TBI. The neuroprotective role might be associated with the preservation of postsynaptic protein expression, the inhibition of activated microglia and the increase in glucose metabolism.
创伤后低温在早期给予时可减轻创伤性脑损伤（TBI）所致的认知缺陷。然而，关于低温预处理对TBI后1个月认知缺陷的影响知之甚少。在本研究中，行为测试显示低温预处理可减轻TBI诱导的小鼠学习和记忆损伤。与正常体温组相比，低温治疗在TBI后1个月显著增加了皮质和海马中PSD93、PSD95和NR2B的表达。低温预处理还恢复了TBI后1个月减少的棘突数量和长时程增强（LTP）损伤，并减少了活化小胶质细胞的数量。另一方面，低温预处理增加了TBI小鼠的葡萄糖代谢。综上所述，这些数据表明低温预处理是预防TBI后棘突丢失、维持正常LTP和保留学习与记忆功能的有效方法。其神经保护作用可能与突触后蛋白表达的保留、活化小胶质细胞的抑制以及葡萄糖代谢的增加有关。
