الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
Depression is the disease of the modern era with rising role of underlying neuroinflammation. Although, microglial activation is crucial for neuroinflammation, the precise molecular mechanism of pro-inflammatory cytokine production of microglia in vivo remains largely elusive. This study was established to investigate the expression of the Wnt/ß-catenin pathway in hippocampal microglia of male Wistar rats exposed to CMS or LPS /CMS models of depression and the effects of lithium on the expression of this pathway as a method to identify a plausible link between exposure to chronic stress and microglial activation. Methods we investigated the effect of chronic administration of Lithium in two different doses on behavioral changes, hippocampal expression of Wnt/β-catenin pathway and microglial activation in male Wistar rats exposed to either CMS or LPS/CMS models of depression. Results: both models induced a depressive-like behaviour in a comparable manner with increased microglial activity and decreased hippocampal expression of the Wnt/β-catenin pathway. chronic treatment with lithium chloride significantly reversed most of the stress induced-behavioural changes with reduction in microglial activation and enhanced hippocampal Wnt/β-catenin pathway expression. Conclusion: This work spotlights the plausible role of the Wnt/β-catenin pathway in regulating microglial activation and subsequent pro-inflammatory changes. This is to deepen our understanding of the mechanism of microglial activation which is thought to be a crucial step in the pathogenesis of depression.
Key words: depression; chronic mild stress; lipopolysaccharide; microglia; lithium; Wnt; β-catenin; neuroinflammation