|星空彩票电脑版
%A WU Bei, WANG Xin-sheng, YANG Yue-ping,TENG Jin-liang %T
Eff ects of Isofl urane On Neurocognitive Function and Its Possible Mechanism%0 Journal Article %D 2015 %J ACTA NEUROPHARMACOLOGICA %R %P 34-39 %V 5 %N 5 %U {http://actanp.hebeinu.edu.cn/CN/abstract/article_279.shtml} %8 2015-10-26 %X A lot of experimental evidences showed that isoflurane can cause the change of learning and cognitive ability，resulting from the inhibition of N-methyl-D-aspartic acid（ NMDA） receptor，depolarization induced by activation of gamma aminobutyric acid（ GABA） receptor，Ca2+ influx and promote activation of caspase-3 which leads to neuronal toxicity. Volatile anesthetics could interfere with physiologic patterns of synaptogenesis and impair density of endritic spines of neurons in the developing cerebral cortex，thus causing changes in behavior. Isoflurane excessively activates calmodulin，inhibits hippocampal synaptic long term potential（ LTP） and curbs short-term memory into long-term memory conversion. Isoflurane induces PERK phosphorylation and increases the expression of CHOP by a series of molecular mechanisms. CHOP up-regulates pro-apoptotic proteins and downregulates anti-apoptotic proteins to promote neuronal apoptosis. Tau protein is highly phosphorylated in the form of nerve fibers and the formation of nerve fibers is considered as a common pathological pathway in the pathogenesis of Alzheimer’s disease. In this review，the mechanism of the general anesthetics inducing consciousness loss and its effect of central nervous system were summarized.