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      Dehydroepiandrosterone Heightens Aggression and Increases Androgen Receptor and Aromatase mRNA Expression in the Brain of a Male Songbird


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          Dehydroepiandrosterone ( DHEA) is a testosterone/oestrogen precursor and known modulator of vertebrate aggression. Male song sparrows ( Melospiza melodia morphna) show high aggression during breeding and nonbreeding life‐history stages when circulating DHEA levels are high, and low aggression during molt when DHEA levels are low. We previously showed that androgen receptor and aromatase mRNA expression are higher during breeding and/or nonbreeding in brain regions associated with reproductive and aggressive behaviour, although the potential role of DHEA in mediating these seasonal changes remained unclear. In the present study, nonbreeding male song sparrows were captured and held in the laboratory under short days (8 : 16 h light/dark cycle) and implanted with s.c. DHEA‐filled or empty (control) implants for 14 days. DHEA implants increased aggression in a laboratory‐based simulated territorial intrusion. Brains of DHEA‐implanted birds showed higher aromatase mRNA expression in the preoptic area ( POA) and higher androgen receptor mRNA expression in the periventricular nucleus of the medial striatum (pv MSt) and ventromedial nucleus of the hypothalamus. The DHEA‐induced increases in aromatase expression in the POA and androgen receptor expression in the pv MSt are consistent with previously reported seasonal increases in these markers associated with naturally elevated DHEA levels. This suggests that DHEA facilitates seasonal increases in aggression in nonbreeding male song sparrows by up‐regulating steroid signalling/synthesis machinery in a brain region‐specific fashion.

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          The vertebrate mesolimbic reward system and social behavior network: a comparative synthesis.

          All animals evaluate the salience of external stimuli and integrate them with internal physiological information into adaptive behavior. Natural and sexual selection impinge on these processes, yet our understanding of behavioral decision-making mechanisms and their evolution is still very limited. Insights from mammals indicate that two neural circuits are of crucial importance in this context: the social behavior network and the mesolimbic reward system. Here we review evidence from neurochemical, tract-tracing, developmental, and functional lesion/stimulation studies that delineates homology relationships for most of the nodes of these two circuits across the five major vertebrate lineages: mammals, birds, reptiles, amphibians, and teleost fish. We provide for the first time a comprehensive comparative analysis of the two neural circuits and conclude that they were already present in early vertebrates. We also propose that these circuits form a larger social decision-making (SDM) network that regulates adaptive behavior. Our synthesis thus provides an important foundation for understanding the evolution of the neural mechanisms underlying reward processing and behavioral regulation. Copyright © 2011 Wiley-Liss, Inc.
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            Distribution of androgen and estrogen receptor mRNA-containing cells in the rat brain: an in situ hybridization study.

            The distribution of cells that express mRNA encoding the androgen (AR) and estrogen (ER) receptors was examined in adult male and female rats by using in situ hybridization. Specific labeling appeared to be largely, if not entirely, localized to neurons. AR and ER mRNA-containing neurons were widely distributed in the rat brain, with the greatest densities of cells in the hypothalamus, and in regions of the telencephalon that provide strong inputs in the medial preoptic and ventromedial nuclei, each of which is thought to play a key role in mediating the hormonal control of copulatory behavior, as well as in the lateral septal nucleus, the medial and cortical nuclei of the amygdala, the amygdalohippocampal area, and the bed nucleus of the stria terminalis. Heavily labeled ER mRNA-containing cells were found in regions known to be involved in the neural control of gonadotropin release, such as the anteroventral periventricular and the arcuate nuclei, but only a moderate density of labeling for AR mRNA was found over these nuclei. In addition, clearly labeled cells were found in regions with widespread connections throughout the brain, including the lateral hypothalamus, intralaminar thalamic nuclei, and deep layers of the cerebral cortex, suggesting that AR and ER may modulate a wide variety of neural functions. Each part of Ammon's horn contained AR mRNA-containing cells, as did both parts of the subiculum, but ER mRNA appeared to be less abundant in the hippocampal formation. Moreover, AR and ER mRNA-containing cells were also found in olfactory regions of the cortex and in both the main and accessory olfactory bulbs. AR and ER may modulate nonolfactory sensory information as well since labeled cells were found in regions involved in the central relay of somatosensory information, including the mesencephalic nucleus of the trigeminal nerve, the ventral thalamic nuclear group, and the dorsal horn of the spinal cord. Furthermore, heavily labeled AR mRNA-containing cells were found in the vestibular nuclei, the cochlear nuclei, the medial geniculate nucleus, and the nucleus of the lateral lemniscus, which suggests that androgens may alter the central relay of vestibular and auditory information as well. However, of all the regions involved in sensory processing, the heaviest labeling for AR and ER mRNA was found in areas that relay visceral sensory information such as the nucleus of the solitary tract, the area postrema, and the subfornical organ. We did not detect ER mRNA in brainstem somatic motoneurons, but clearly labeled AR mRNA-containing cells were found in motor nuclei associated with the fifth, seventh, tenth, and twelfth cranial nerves. Similarly, spinal motoneurons contained AR but not ER mRNA.(ABSTRACT TRUNCATED AT 400 WORDS)
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              Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS).

              DHEA and DHEAS are steroids synthesized in human adrenals, but their function is unclear. In addition to adrenal synthesis, evidence also indicates that DHEA and DHEAS are synthesized in the brain, further suggesting a role of these hormones in brain function and development. Despite intensifying research into the biology of DHEA and DHEAS, many questions concerning their mechanisms of action and their potential involvement in neuropsychiatric illnesses remain unanswered. We review and distill the preclinical and clinical data on DHEA and DHEAS, focusing on (i) biological actions and putative mechanisms of action, (ii) differences in endogenous circulating concentrations in normal subjects and patients with neuropsychiatric diseases, and (iii) the therapeutic potential of DHEA in treating these conditions. Biological actions of DHEA and DHEAS include neuroprotection, neurite growth, and antagonistic effects on oxidants and glucocorticoids. Accumulating data suggest abnormal DHEA and/or DHEAS concentrations in several neuropsychiatric conditions. The evidence that DHEA and DHEAS may be fruitful targets for pharmacotherapy in some conditions is reviewed.

                Author and article information

                J Neuroendocrinol
                J. Neuroendocrinol
                Journal of Neuroendocrinology
                John Wiley and Sons Inc. (Hoboken )
                09 December 2016
                December 2016
                : 28
                : 12 ( doiID: 10.1111/jne.2016.28.issue-12 )
                : n/a
                [ 1 ] School of STEM (Division of Biological Sciences)University of Washington Bothell Bothell WAUSA
                [ 2 ] BiologySeattle University Seattle WAUSA
                [ 3 ] Biology DepartmentRadford University Radford VAUSA
                [ 4 ]The Roslin Institute and Royal (Dick) School of Veterinary Studies University of Edinburgh EdinburghUK
                [ 5 ] College of Biological SciencesUniversity of California Davis Davis CA USA
                Author notes
                [*] [* ]Correspondence to: Douglas W. Wacker, School of STEM (Biological Sciences Division), University of Washington Bothell, 18115 Campus Way NE, Box 358538, Bothell, WA 98011, USA (e‐mail: dwacker@ 123456uw.edu ).
                © 2016 The Authors. Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology

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

                : 25 August 2016
                : 04 October 2016
                : 30 October 2016
                Page count
                Figures: 6, Tables: 0, Pages: 9, Words: 6636
                Funded by: National Science Foundation (NSF)
                Award ID: IBN‐0317141
                Funded by: Biotechnology and Biological Sciences Research Council
                Award ID: BB/J004316/1
                Award ID: BB/J004332/1
                Funded by: Society for Comparative and Integrative Biology (SICB) Grant‐in‐Aid of Research
                Funded by: NSF Research Coordination Network
                Award ID: E‐BIRD‐USA
                Funded by: NSF Graduate Research Fellowship
                Original Article
                Original Articles
                Custom metadata
                December 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.7 mode:remove_FC converted:24.02.2017

                Endocrinology & Diabetes
                dehydroepiandrosterone,aromatase,androgen receptor,aggression,sparrow
                Endocrinology & Diabetes
                dehydroepiandrosterone, aromatase, androgen receptor, aggression, sparrow


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