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- W2034213956 abstract "The field of biological psychiatry has been hindered by the paucity of animal models of depression and bipolar disorder that are reliable across laboratories, assess constructs with relevance to core symptomatology of these disorders, and include inducing conditions that are based on solid theoretical rationales about the etiologies of these disorders. Two studies published in this issue of Biological Psychiatry used molecular genetic techniques in rodents to reveal previously unidentified mechanisms involved in the neurobiological regulation of mood and affect, moving beyond the traditional targets of current pharmacotherapies. These studies suggest roles for γ-aminobutyric acid (GABA) A receptor and Circadian Locomotor Output Cycles Kaput transcription factor in depression and bipolar disorder. Because malfunctions in such regulatory mechanisms lead to affective symptoms of depression and mania, these findings provide new insights regarding the etiology of mood dysregulation and its potential treatment. γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of DepressionBiological PsychiatryVol. 68Issue 6PreviewThe γ-aminobutyric acid (GABA) Type A receptor deficits that are induced by global or forebrain-specific heterozygous inactivation of the γ2 subunit gene in mouse embryos result in behavior indicative of trait anxiety and depressive states. By contrast, a comparable deficit that is delayed to adolescence is without these behavioral consequences. Here we characterized γ2-deficient mice with respect to hypothalamic-pituitary-adrenal (HPA) axis abnormalities and antidepressant drug responses. Full-Text PDF" @default.
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- W2034213956 date "2010-09-01" @default.
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- W2034213956 title "Studies in Genetically Modified Mice Suggest Novel Mechanisms of Mood Regulation" @default.
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- W2034213956 doi "https://doi.org/10.1016/j.biopsych.2010.07.020" @default.
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