Glucocorticoid receptor overexpression in forebrain: a mouse model of increased emotional lability. - Wikidata - wikimedia - TriplyDB

Glucocorticoid receptor overexpression in forebrain: a mouse model of increased emotional lability.

Glucocorticoid receptor overexpression in forebrain: a mouse model of increased emotional lability.

http://www.wikidata.org/entity/Q37416316

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The Neurobiology of the Switch Process in Bipolar Disorder Mechanisms of stress in the brain Transcriptional regulation of the 5-HT1A receptor: implications for mental illness Antecedents and consequences of drug abuse in rats selectively bred for high and low response to novelty New approaches to antidepressant drug discovery: beyond monoamines 50 years of hurdles and hope in anxiolytic drug discovery Luman/CREB3 recruitment factor regulates glucocorticoid receptor activity and is essential for prolactin-mediated maternal instinct Neural regulation of endocrine and autonomic stress responses Single prolonged stress enhances hippocampal glucocorticoid receptor and phosphorylated protein kinase B levels Adrenal activity during repeated long-access cocaine self-administration is required for later CRF-Induced and CRF-dependent stressor-induced reinstatement in rats.Annual Research Review: Transgenic mouse models of childhood-onset psychiatric disorders.The clinical implications of mouse models of enhanced anxiety.Hypothalamic-pituitary-adrenal axis dysregulation and behavioral analysis of mouse mutants with altered glucocorticoid or mineralocorticoid receptor function Reverse translational strategies for developing animal models of bipolar disorder.An affective disorder in zebrafish with mutation of the glucocorticoid receptor.Dynamic transcriptomic response to acute hypertension in the nucleus tractus solitarius.GPR3 receptor, a novel actor in the emotional-like responses Transcriptional effects of glucocorticoid receptors in the dentate gyrus increase anxiety-related behaviors.Cellular mechanisms underlying affective resiliency: the role of glucocorticoid receptor- and mitochondrially-mediated plasticity.Glucocorticoid receptor deletion from the dorsal raphé nucleus of mice reduces dysphoria-like behavior and impairs hypothalamic-pituitary-adrenocortical axis feedback inhibition Acquired deficit of forebrain glucocorticoid receptor produces depression-like changes in adrenal axis regulation and behavior Vmat2 heterozygous mutant mice display a depressive-like phenotype.Prenatal thyroxine treatment disparately affects peripheral and amygdala thyroid hormone levels.Differences in mouse maternal care behavior - is there a genetic impact of the glucocorticoid receptor?Forebrain glucocorticoid receptor overexpression increases environmental reactivity and produces a stress-induced spatial discrimination deficit FGF2 is a target and a trigger of epigenetic mechanisms associated with differences in emotionality: partnership with H3K9me3.Mood, food, and obesity.Forebrain glucocorticoid receptor gene deletion attenuates behavioral changes and antidepressant responsiveness during chronic stress.Transient early-life forebrain corticotropin-releasing hormone elevation causes long-lasting anxiogenic and despair-like changes in mice Translational research in bipolar disorder: emerging insights from genetically based models.Dissection of corticotropin-releasing factor system involvement in locomotor sensitivity to methamphetamine Linking molecules to mood: new insight into the biology of depression.Modifications of glucocorticoid receptors mRNA expression in the hypothalamic-pituitary-adrenal axis in response to early-life stress in female Japanese quail.Partial rodent genetic models for bipolar disorder.Abnormal development of monoaminergic neurons is implicated in mood fluctuations and bipolar disorder.Experimental models of stress.Expression and localization of type II diacylglycerol kinase isozymes δ and η in the developing mouse brain.Early-life forebrain glucocorticoid receptor overexpression increases anxiety behavior and cocaine sensitization.Mineralocorticoid receptor overexpression in forebrain decreases anxiety-like behavior and alters the stress response in mice.Inborn differences in environmental reactivity predict divergent diurnal behavioral, endocrine, and gene expression rhythms.

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Glucocorticoid receptor overexpression in forebrain: a mouse model of increased emotional lability.

http://www.wikidata.org/entity/Q37416316

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article científic

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 27 July 2004

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Glucocorticoid receptor overex ...... increased emotional lability.

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Glucocorticoid receptor overex ...... increased emotional lability.

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type

label

Glucocorticoid receptor overex ...... increased emotional lability.

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Glucocorticoid receptor overex ...... increased emotional lability.

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Glucocorticoid receptor overex ...... increased emotional lability.

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Glucocorticoid receptor overex ...... increased emotional lability.

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PNAS.0402208101

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Proceedings of the National Academy of Sciences of the United States of America

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Glucocorticoid receptor overex ...... increased emotional lability.

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Audrey F Seasholtz

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Gwen Schafer

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Huda Akil

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Kun-Ruey Shieh

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Li Liu

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Qiang Wei

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Sharon Burke

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Stanley J Watson

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Terry E Robinson

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Xin-Yun Lu

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P2860

Plasma membrane monoamine transporters: structure, regulation and function

Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants

Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety

Control of memory formation through regulated expression of a CaMKII transgene

Brain corticosteroid receptor balance in health and disease

A role for corticotropin releasing factor and urocortin in behavioral responses to stressors.

Corticosteroids in relation to fear, anxiety and psychopathology.

The corticosteroid receptor hypothesis of depression.

The hippocampus mediates glucocorticoid-induced impairment of spatial memory retrieval: dependence on the basolateral amygdala.

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