The exploration of genes related to depression using an animal model.
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Accession number;02A0472899
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| Title;The exploration of genes related to depression using an animal model. |
| Author;
NAKATANI NORIAKI
(Inst. Physical and Chemical Res. (RIKEN), Brain Sci. Inst., JPN)
ABURATANI HIROYUKI
(Todai Sentankagakugikense Genomusaiensu)
IIJIMA YUKI
(Inst. Physical and Chemical Res. (RIKEN), Brain Sci. Inst., JPN)
SEMBA JUN'ICHI
(Univ. of Air, Fac. of Liberal Arts)
YOSHIKAWA TAKEO
(Inst. Physical and Chemical Res. (RIKEN), Brain Sci. Inst., JPN)
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Journal Title;Annual Report of the Pharmacopsychiatry Research Foundation
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Journal Code:Y0939A
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ISSN:0286-7591
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VOL.;NO.34;PAGE.229-236(2002)
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| Figure&Table&Reference;FIG.2, TBL.2, REF.15 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Depression is one of major psychoses with a particular set of symptoms, including depressed mood, a loss of interest, diminished appetite and loss of weight, sleep disturbances and psychomotor retardation. There are cumulative data suggesting that depression has genetic components in its etiology. However, definitive susceptibility genes remain unidentified. To elucidate the mechanism of depression, we performed a genome-wide gene expression analysis, using gene chips and an animal model of depression, learned helplessness(LH) rats. The genes whose expressions showed significant alteration in LH group, compared with controls and antidepressant-treated group were selected using Venn-diagrams. They were clustered into groups based on possible biological functions. The gene members categorized into receptors and ion channels were all attenuated in both frontal cortex and hippocampus of LH animals. These results suggest that a reduced intracellular signal transduction caused by the decreased expression of genes coding receptors and ion channels may underlie the pathophysiology of depression. (author abst.) |
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