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  • 2000-2004  (3)
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Material
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Year
  • 1
    Electronic Resource
    Electronic Resource
    Androgens Alter Corticotropin Releasing Hormone and Arginine Vasopressin mRNA Within Forebrain Sites Known to Regulate Activity in the Hypothalamic-Pituitary-Adrenal Axis (2001)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 13 (2001), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To reveal direct effects of androgens, independent of glucocorticoids, we studied the effects of gonadectomy (GDX) in adrenalectomized (ADX) rats with or without androgen replacement on corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) mRNA expression within various forebrain sites known to regulate the hypothalamic-pituitary-adrenal axis. These included the medial parvocellular portion of the paraventricular nucleus of the hypothalamus (mp PVN), the central and medial nuclei of the amygdala and bed nuclei of the stria terminalis (BNST). In the mp PVN, ADX stimulated both CRH and AVP mRNA expression. Combined ADX + GDX inhibited only AVP, and testosterone and dihydrotestosterone (DHT) restored AVP mRNA. In the central nucleus of the amygdala, ADX decreased CRH mRNA expression, and this response was unaffected by GDX ± testosterone or DHT replacement. In the medial amygdala, AVP mRNA expression was decreased by ADX, abolished by ADX + GDX, and restored by androgen replacement. ADX had no effect on CRH and AVP mRNA expression in the BNST. GDX + ADX, however, reduced CRH mRNA expression only within the fusiform nuclei of the BNST and reduced the number of AVP-expressing neurones in the posterior BNST. Androgen replacement reversed both responses. In summary, in ADX rats, AVP, but not CRH mRNA expression in the amygdala and mp PVN, is sensitive to GDX ± androgen replacement. Both CRH- and AVP-expressing neurones in the BNST respond to GDX and androgen replacement, but not to ADX alone. Because androgen receptors are not expressed by hypophysiotropic PVN neurones, we conclude that glucocorticoid-independent, androgenic influences on medial parvocellular AVP mRNA expression are mediated upstream from the PVN, and may involve AVP-related pathways in the medial amygdala, relayed to and through CRH- and AVP-expressing neurones of the BNST.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2001.00653.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Sucrose Intake and Corticosterone Interact with Cold to Modulate Ingestive Behaviour, Energy Balance, Autonomic Outflow and Neuroendocrine Responses During Chronic Stress (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In adrenalectomized (ADX) rats, either corticosterone replacement or increased sucrose intake will restore body weight gain, uncoupling protein-1, fat depot mass, food intake and corticotropin-releasing factor mRNA expression to normal. Here, we tested the potential interactions between sucrose intake and circulating corticosterone on behavioural, metabolic, autonomic and neuroendocrine responses to the stress of cold. Rats were left intact, sham-ADX, or ADX and replaced with pellets that provided normal, basal (30%B) or high stress (100%B) constant circulating concentrations of corticosterone ± sucrose. More calories were consumed in cold than at room temperature (RT), provided that corticosterone concentrations were elevated above mean daily basal values in cold. Neither increased sucrose nor increased chow ingestion occurred in cold if the rats were ADX and replaced with 30%B. However, sucrose drinking in this group markedly ameliorated other responses to cold. By contrast, ADX30%B rats not drinking sucrose fared poorly, and none of the metabolic or endocrine variables were similar to those in sham-ADX controls. ADX100%B group in cold, resembled intact rats without sucrose; however, this group was metabolically abnormal at RT. We conclude that drinking sucrose lowers stress-induced corticosterone secretion while reducing many responses to cold; elevated corticosterone concentrations in the stress-response range are essential for the normal integrated cold-induced responses to occur.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2002.00784.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Corticosterone Exerts Site-Specific and State-Dependent Effects in Prefrontal Cortex and Amygdala on Regulation of Adrenocorticotropic Hormone, Insulin and Fat Depots (2001)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 13 (2001), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Chronic stress stimulates corticosterone secretion and recruits brain pathways that regulate energy balance (caloric acquisition and deposition) and facilitate hypothalamic-pituitary-adrenal responsiveness to new stressors. We implanted corticosterone or cholesterol bilaterally either near the central nucleus of the amygdala (CeA) or in the prefrontal cortex to determine whether high concentrations of the steroid act at either site, with or without chronic stress. Rats were adrenalectomized and treated systemically with low doses of corticosterone. Half were maintained at room temperature and the other half were exposed to 5 °C cold for 5 days before all rats were restrained. There was limited diffusion of corticosterone from brain implants. Corticosterone in prefrontal cortex, but not CeA, decreased plasma insulin and adrenocorticotropic hormone (ACTH) responses to acute restraint in both control and chronically cold stressed rats. Corticosterone implants near CeA decreased the weight of fat depots only in cold; corticosterone implants in prefrontal cortex were ineffective. We conclude that (i) corticosterone inhibits insulin and ACTH secretion by an action in prefrontal cortex but not CeA; (ii) high concentrations of corticosterone secreted during chronic stress alter metabolism through (autonomic) outputs of the CeA and prefrontal cortex in site- and variable-specific fashion; and (iii) the amygdala is a component of a stress-recruited, state-dependent pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2001.00676.x
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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