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Some anesthetics have been suggested to induce Alzheimer's disease (AD) neuro-pathogenesis. Increasing evidence indicates that hyperphosphorylated tau plays a key role in the pathogenic events that occur in AD. Isoflurane has been shown to induce apoptosis, which leads to accumulation of amyloid-β (Aβ). We set out to investigate whether isoflurane can induce apoptosis by increasing hyperphosphorylated tau in Aβ-induced cells and the underlying mechanism. Cultured rat pheochromocytoma cells (PC12) were exposed to 20 mM Aβ alone or with 2 % isoflurane for 6 h. The cell viability was determined by MTT assay, and the apoptosis rate was detected by flowcytometry. Western blotting and immunocytochemical staining were performed to observe the protein expression of Bcl-2 family, tau phosphorylation of different sites, tau protein kinases and phosphatases. Additionally, lithium chloride was administered to all above groups to investigate the changes of apoptosis rate and protein expression. The apoptosis rate was significantly increased in Aβ group compared with the others groups, which was accompanied by bcl-2 decline, and the phosphorylation of glycogen synthase kinase-3β(GSK-3β) and tau of two sites increased. LiCl attenuated the cellular apoptosis by inhibition the level of tau phosphorylation. Isoflurane upregulated the level of phosphorylated GSK-3β, which phosphorylate tau at different sites, and aggravated the apoptotic rate of the Aβ-induced PC12 cells. It indicated that isoflurane-induced tau phosphorylation might play a role in the AD-like development. [ABSTRACT FROM AUTHOR]

Depressive disorders are devastating metal illness that can lead to deterioration in the social and occupational functioning of affected individuals. The etiology and pathophysiology of depression remain unknown. Present study was performed to better understand the underlying causes of depression. An experimental animal depression was induced in male BALB/c mice subjected to a chronic mild stress (CMS) procedure involving different stressor for consecutive 4 weeks. A cDNA microarray was employed to study the effects of CMS on the gene expression in cerebral cortex and hippocampus. 4-week CMS caused a significant reduction of 2% sucrose consumption. Morris water maze procedure showed impairment in cognitive function in stressed mice. Results of microarray showed that there were 102 and 60 genes were markedly affected by CMS treatment in cerebral cortex and hippocampus regions, respectively, including DNA damage/repair-related enzymes, anti-oxidant enzyme, and cyclin and cyclin-dependent kinase (CDK). These findings suggest that multiple biochemical effects play an important role the etiology of depression. [ABSTRACT FROM AUTHOR]