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      Effects of Estrogen Treatment on Expression of Brain-Derived Neurotrophic Factor and cAMP Response Element-Binding Protein Expression and Phosphorylation in Rat Amygdaloid and Hippocampal Structures

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          Clinical studies indicate an effect of estrogen (E<sub>2</sub>) on affect and cognition, which may be mediated by the cAMP response element-binding protein (CREB) pathway and CREB-related gene target brain-derived neurotrophic factor (BDNF). We investigated the effect of E<sub>2</sub> on CREB expression and phosphorylation and BDNF expression in the amygdala and hippocampus, areas involved in emotional processing. Ovariectomized rats were given 10 µg 17β-estradiol or vehicle for 14 days and expression of components of the CREB signaling pathway, i.e., CREB, phosphorylated CREB (pCREB), and BDNF in amygdala and hippocampus were investigated using immunogold labeling. Levels of BDNF mRNA were determined by in situ reverse-transcriptase polymerase chain reaction. We also examined the effect of E<sub>2</sub> on calcium/calmodulin kinase (CaMK IV) immunolabeling in the hippocampus. E<sub>2</sub> increased immunolabeling and mRNA levels of BDNF in the medial and basomedial amygdala and CA1 and CA3 regions of the hippocampus, but not in any other amygdaloid or hippocampal regions examined. E<sub>2</sub> increased immunolabeling of CREB and pCREB in the medial and basomedial, but not central or basolateral amygdala. E<sub>2</sub> also increased CaMK IV and pCREB immunolabeling in the CA1 and CA3 regions, but not CA2 region or dentate gyrus, of the hippocampus. There was no change in immunolabeling of CREB in any hippocampal region. These data identify a signaling pathway through which E<sub>2</sub> increases BDNF expression that may underlie some actions of E<sub>2</sub> on affective behavior and indicate neuroanatomical heterogeneity in the E<sub>2</sub> effect within the amygdala and hippocampus.

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          Most cited references 61

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          The BDNF val66met Polymorphism Affects Activity-Dependent Secretion of BDNF and Human Memory and Hippocampal Function

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            Behavioural despair in rats: a new model sensitive to antidepressant treatments.

            Rats when forced to swim in a cylinder from which they cannot escape will, after an initial period of vigorous activity, adopt a characteristic immobile posture which can be readily identified. Immobility was reduced by various clinically effective antidepressant drugs at doses which otherwise decreased spontaneous motor activity in an open field. Antidepressants could thus be distinguished from psychostimulants which decreased immobility at doses which increased general activity. Anxiolytic compounds did not affect immobility whereas major tranquilisers enhanced it. Immobility was also reduced by electroconvulsive shock, REM sleep deprivation and "enrichment" of the environment. It was concluded that immobility reflects a state of lowered mood in the rat which is selectively sensitive to antidepressant treatments. Positive findings with atypical antidepressant drugs such as iprindole and mianserin suggest that the method may be capable of discovering new antidepressants hitherto undetectable with classical pharmacological tests.
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              CREB and memory.

              The cAMP responsive element binding protein (CREB) is a nuclear protein that modulates the transcription of genes with cAMP responsive elements in their promoters. Increases in the concentration of either calcium or cAMP can trigger the phosphorylation and activation of CREB. This transcription factor is a component of intracellular signaling events that regulate a wide range of biological functions, from spermatogenesis to circadian rhythms and memory. Here we review the key features of CREB-dependent transcription, as well as the involvement of CREB in memory formation. Evidence from Aplysia, Drosophila, mice, and rats shows that CREB-dependent transcription is required for the cellular events underlying long-term but not short-term memory. While the work in Aplysia and Drosophila only involved CREB function in very simple forms of conditioning, genetic and pharmacological studies in mice and rats demonstrate that CREB is required for a variety of complex forms of memory, including spatial and social learning, thus indicating that CREB may be a universal modulator of processes required for memory formation.

                Author and article information

                S. Karger AG
                October 2005
                02 November 2005
                : 81
                : 5
                : 294-310
                aDepartment of Anatomy and Cell Biology and bDepartment of Psychiatry, University of Illinois at Chicago, and cJesse Brown Veterans Affairs Medical Center, Chicago, Ill., USA
                88448 PMC1343485 Neuroendocrinology 2005;81:294–310
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 5, References: 102, Pages: 17
                Original Paper


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