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Depression is one of the most common and most devastating psychiatric disorders. Despite its high prevalence and socio-economic impact, little is known about its etiology. Preclinical and clinical studies have demonstrated that depression can lead to cell loss and atrophy in limbic brain structures including hippocampus. An emerging hypothesis suggests that the treatment of depression is likely to involve a plasticity of neuronal pathway. Although a variety of treatment strategies is available. A major problem in its therapy consists of unpredictability of its drug response. Antidepressant treatments may exert their therapeutic effects by stimulating appropriate adaptive changes in neuronal systems. A novel therapeutic approach consists of targeting signal transduction and gene expression pathways. One of the best investigated pathways is cyclic AMP messenger system which ultimately influences gene expression by activating the transcription factor cyclic AMP response element binding protein (CREB) via phosphorylation. Recent studies have demonstrated that cyclic AMPCREB system is disturbed in depression. This review focuses on the molecular mechanism underlying the effects of antidepressant treatment including adaptations in the cyclic AMP transduction cascade and also suggests that increased CREB activity may result in an improved neuronal plasticity, which in turn could contribute to amelioration of the clinical symptoms of depression.
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Author(s): Sanjukta Misra
Depression, Cyclic AMP transduction cascade, Cyclic AMP response element binding protein, antidepressant treatment