1,721,927 research outputs found

    Prenatal exposure of mice to an environmental estrogen alters sex differences in brain and behavior

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    56. PRENATAL EXPOSURE OF MICE TO A LOW-DOSE ENVIRONMENTAL ESTROGEN ALTERS SEX DIFFERENCES IN BRAIN AND BEHAVIOR. Palanza; P:; Ponzi, D., Gioiosa, L., Flugge, G., Parmigiani, S., and Fuchs, E. Dipartimento di Biologia Evolutiva, Universita` di Parma. Laboratory of Neurobiology, German Primate Center, Goettingen. The presence in the environment to a large number of environmental and industrial compounds that have estrogenic activity (Environmental Estrogens, EE) raises major health concerns. Sexually dimorphic behaviors are particularly useful to study the effects of low concentrations of EE, similar to environmental contamination, because they are highly sensitive to alterations of the endocrine mileu. Behavior is the endpoint of complex, integrated systems and therefore is a good biomarker of neuroendocrine and neurobiological alterations. We investigated the effects of prenatal exposure (via maternal treatment) to an environmental-like, low dose of bisphenol A (BPA, an estrogenic compound used in food industry) on mice behavioral response to novelty and on the noradrenergic system in the brain. Mice were tested in a free-choice novelty preference test at adolescence, in a freeexploratory open field and elevated plus-maze (EPM) as adults. Both adolescent and adult mice exposed to BPAshowed either a decrease or a reversion in sexual differences in response to novelty. Contrary to the control profile, BPA-exposed males and females did not differ in exploration, an effect due mainly to changes in BPA-exposed females relative to controls. As adults, mice were sacrificed and their brain were analyzed for alpha2 adrenergic receptor system in locus coeruleus (LC) and preoptic area (PO). Control mice showed a sexually dimorphic profile of receptor density in the PO, while prenatal BPA-exposure lowered such sex differences; BPA-exposed males showed increased receptors number, thus resulting more similar to the control females’ profile. In both the PO and LC of exposed animals, a decreased affinity of alpha2-adrenergic receptors was observed

    Examining novel concepts of the pathophysiology of depression in the chronic psychosocial stress paradigm in tree shrews

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    Despite decades of research on psychiatric disorders, the aetiology and precise biological mechanisms that underlie depressive diseases are still poorly understood. There is increasing evidence that psychiatric disorders not only have a neurochemical basis but are also associated with morphological alterations in central nervous neurons and/or glial cells. Antidepressants may act by restoring structure as well as function of neural networks, meaning that they may, as a fundamental principle, affect neural plasticity underlying normal brain functioning. To examine these novel concepts of the pathophysiology of depression and antidepressant medication we have carried out a series of experiments using the chronic psychosocial stress paradigm in male tree shrews, an animal model with a high validity for the pathophysiology of depressive disorders, in which the animals were treated with the tricyclic antidepressant compound clomipramine. We found that one month of stress reduced cell proliferation in the dentate gyrus, and decreased the total hippocampal volume. Gene transcription analysis revealed that, under these experimental conditions, expression of genes known to be involved in processes of cell differentiation is suppressed. These effects of social conflict on hippocampal cells, including gene transcription, and on the entire hippocampal volume could be counteracted by chronic treatment with the antidepressant clomipramine. Stress also induced a constant hyperactivity of the hypothalamic-pituitary-adrenal axis, and suppressed both motor and marking behaviour. These neuroendocrine and behavioural stress-induced changes were also re-normalized by clomipramine. (C) 2004 Lippincott Williams Wilkins

    Remodeling of neuronal networks by stress

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    Stress can be a threat to the physiological and psychological integrity of an individual and may result in psychic and behavioral changes. The stress response is mediated through in-concert activity of many brain areas and there is experimental evidence that stress induces structural changes in neuronal networks, in particular in the hippocampus, the prefrontal cortex and the amygdala. Within the hippocampal formation, stress exposure results in remodeling of dendrites of the CA3 pyramidal neurons and in reduced numbers of synapses on these neurons. Furthermore, stress inhibits adult neurogenesis in the dentate gyrus and appears to modulate the GABAergic system. In the prefrontal cortex, repeated exposure to stress causes dendritic retraction and loss of spines in pyramidal neurons whereas in the amygdala stress can elicit dendritic hypertrophy. These microscopically detectable changes in neuronal structures indicate the reorganization of neuronal networks. Moreover, molecular studies show that stress modulates expression of genes involved in neuronal differentiation and/or structural remodeling. Since a wealth of data documents the adverse effects of stress on emotions and cognition these alterations are commonly interpreted as the deleterious effect of chronic stress on the central nervous system. However, it is also possible that at least part of these changes reflect adaptive responses, as the network system rearranges its connections in order to cope with the changing requirements from the internal or external environment

    Preclinical approaches to examine novel concepts of the pathophysiology of depressive disorders: Lessons learned from tree shrews

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    Recent studies have provided evidence that mood disorders such as major depression not only have a neurochemical basis but are also associated with alterations in neuronal and glial Structures. Anti depressants may act by restoring structure as well as function of neural networks meaning that they may, as a fundamental principle, affect neural Plasticity underlying normal brain functioning. To examine this novel concept of the pathophysiology of depression and antidepressant medication, we have carried Out I series of experiments using the social stress paradigm in tree shrews, an animal model with a high validity for the pathophysiology of major depression. We found that 1 month of stress reduced the proliferation rate of newly born neurons in the dentate gyrus and decreased hippocampal volume. Notably, the suppressive effects of social conflict stress on hippocampal structure could be counteracted by treatments with different antidepressants such as clomipramine, tianeptine, and the selective NK1 receptor antagonists L-760735. In addition, the stress-induced decrease in number of parvalbumin-containing cells in the hippocampal formation, presumably GABAergic interneurons, was prevented by concomitant treatment with fluoxetine. These studies show that different classes of antidepressants can reverse the structural alterations of the hippocampal formation induced by stress

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Variations on the Author

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    “Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
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