| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Although dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis by chronic stress is indicative of major depression, the molecular mechanisms and functional changes in the brain underlying depression are largely unknown. In this study, by using chronic stress for mice, we attempted to elucidate the molecular pathway induced by elevated plasma corticosterone levels. We observed the following effects both, in vivo and in vitro: (1) repeated exposure to stress activates the 3-phosphoinositide-dependent protein kinase (PDK1)-serum glucocorticoid regulated kinase (SGK1)-N-myc downstream-regulated gene 1 (NDRG1)-adhesion molecule stabilization pathway via an increase in plasma corticosterone levels; and (2) the activation of this signaling pathway induces morphological changes in oligodendrocytes. Our data strongly suggest that these abnornalities of oligodendrocytes are possibly related to depression-like symptoms.
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