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      Potential Antidepressant Role of Neurotransmitter CART: Implications for Mental Disorders

      review-article
      1, 2 , *
      Depression Research and Treatment
      Hindawi Publishing Corporation

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          Abstract

          Depression is one of the most prevalent and debilitating public health concerns. Although no single cause of depression has been identified, it appears that interaction among genetic, epigenetic, biochemical, environmental, and psychosocial factors may explain its etiology. Further, only a fraction of depressed patients show full remission while using current antidepressants. Therefore, identifying common pathways of the disorder and using that knowledge to develop more effective pharmacological treatments are two primary targets of research in this field. Brain-enriched neurotransmitter CART (cocaine- and amphetamine-regulated transcript) has multiple functions related to emotions. It is a potential neurotrophic factor and is involved in the regulation of hypothalamic-pituitary-adrenal axis and stress response as well as in energy homeostasis. CART is also highly expressed in limbic system, which is considered to have an important role in regulating mood. Notably, adolescents carrying a missense mutation in the CART gene exhibit increased depression and anxiety. Hence, CART peptide may be a novel promising antidepressant agent. In this paper, we summarize recent progress in depression and CART. In particular, we emphasize a new antidepressant function for CART.

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          Most cited references107

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          A neurotrophic model for stress-related mood disorders.

          There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.
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            Neurobiology of Depression

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              The global burden of disease, 1990-2020.

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                Author and article information

                Journal
                Depress Res Treat
                DRT
                Depression Research and Treatment
                Hindawi Publishing Corporation
                2090-1321
                2090-133X
                2011
                7 July 2011
                : 2011
                : 762139
                Affiliations
                1The Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
                2The Department of Public Health and Preventive Medicine, the Knight Cancer Institute, Oregon Health and Science University, Portland, OR 97239, USA
                Author notes
                *Peizhong Mao: maop@ 123456ohsu.edu

                Academic Editor: Ronald S. Duman

                Article
                10.1155/2011/762139
                3138108
                21785720
                4021e280-adc0-4cdc-92f6-3b8930cac4f3
                Copyright © 2011 Peizhong Mao.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 February 2011
                : 20 April 2011
                : 16 May 2011
                Categories
                Review Article

                Neurology
                Neurology

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