Mechanism underlying the glucocorticoid-decreased function of neurotrophic factor in depression.
Project/Area Number |
21680034
|
Research Category |
Grant-in-Aid for Young Scientists (A)
|
Allocation Type | Single-year Grants |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | National Center of Neurology and Psychiatry |
Principal Investigator |
NUMAKAWA Tadahiro 独立行政法人国立精神・神経医療研究センター, 神経研究所疾病研究第3部, 室長 (40425690)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥26,260,000 (Direct Cost: ¥20,200,000、Indirect Cost: ¥6,060,000)
Fiscal Year 2011: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥8,710,000 (Direct Cost: ¥6,700,000、Indirect Cost: ¥2,010,000)
Fiscal Year 2009: ¥13,130,000 (Direct Cost: ¥10,100,000、Indirect Cost: ¥3,030,000)
|
Keywords | 精神 / 神経疾患の病態と治療 / 神経科学 / 脳神経疾患 / 細胞・組織 |
Research Abstract |
Following glucocorticoid(stress hormone) exposure, BDNF-dependent synaptic maturation was decreased in cultured cortical neurons. We found that shp2-TrkB interaction, which is important for BDNF-mediated synaptic protein expression, was also reduced. In vivo models, we examined possible change of BDNF-related intracellular signaling in forebrain after restraint stress. We found that significant GR downregulation after restraint operation and confirmed a decrease in BDNF-stimulated neurotransmitter release.
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Report
(4 results)
Research Products
(75 results)