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      The Selective Glucocorticoid Receptor Antagonist ORG 34116 Decreases Immobility Time in the Forced Swim Test and Affects cAMP-Responsive Element-Binding Protein Phosphorylation in Rat Brain

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          Glucocorticoid receptor (GR) antagonists can block the retention of the immobility response in the forced swimming test. Recently, we showed that forced swimming evokes a distinct spatiotemporal pattern of cAMP-responsive element-binding protein (CREB) phosphorylation in the dentate gyrus (DG) and neocortex. In the present study, we found that chronic treatment of rats with the selective GR antagonist ORG 34116 decreased the immobility time in the forced swim test, increased baseline levels of phosphorylated CREB (P-CREB) in the DG and neocortex and affected the forced swimming-induced changes in P-CREB levels in a time- and site-specific manner. Overall, we observed that, in control rats, forced swimming evoked increases in P-CREB levels in the DG and neocortex, whereas in ORG 34116-treated animals a major dephosphorylation of P-CREB was observed. These observations underscore an important role of GRs in the control of the phosphorylation state of CREB which seems to be of significance for the immobility response in the forced swim test and extend the molecular mechanism of action of GRs in the brain.

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            Function and regulation of CREB family transcription factors in the nervous system.

            CREB and its close relatives are now widely accepted as prototypical stimulus-inducible transcription factors. In many cell types, these factors function as effector molecules that bring about cellular changes in response to discrete sets of instructions. In neurons, a wide range of extracellular stimuli are capable of activating CREB family members, and CREB-dependent gene expression has been implicated in complex and diverse processes ranging from development to plasticity to disease. In this review, we focus on the current level of understanding of where, when, and how CREB family members function in the nervous system.
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              Neurobiology of Depression


                Author and article information

                S. Karger AG
                July 2005
                06 July 2005
                : 81
                : 2
                : 129-136
                aMax Planck Institute of Psychiatry, Section of Neuropsychopharmacology, Munich; bDepartment of Clinical Neurophysiology, University of Göttingen, and Department of Molecular Cell Biology, Max Planck Institute of Biophysical Chemistry, Göttingen, Germany; cHenry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), University of Bristol, Bristol, UK
                86413 Neuroendocrinology 2005;81:129–136
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 4, References: 38, Pages: 8
                Original Paper


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