| Project/Area Number |
16590187
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
|
|---|
| Research Institution | Tokyo Metropolitan Institute of Gerontology |
|---|
Principal Investigator |
HOTTA Harumi Tokyo Metropolitan Institute of Gerontology, Senior Researcher, 東京都老人総合研究所, 主任研究員 (70199511)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
UCHIDA Sae Tokyo Metropolitan Institute of Gerontology, Researcher, 東京都老人総合研究所, 研究員 (90270660)
|
|---|
| Project Period (FY) |
2004 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | BDNF / basal forebrain / cerebral cortex / electrical stimulation / ELISA / rat / 細胞外液 |
|---|
| Research Abstract |
The effect of electric stimulation of the basal forebrain on the neurotrophic factors in the cerebral cortex was examined. Among neurotrophines found in the cerebral cortex, we focused on brain-derived neurotrophic factor (BDNF) that it known to have a protective action against cerebral ischemia. A neuropeptide dyalisis probe was implanted in the cerebral cortex of parietal lobe using halothane-anesthetized rats. Extracellular fluid was collected every 100 minutes, for 800 minutes. Concentration of BDNF in the collected samples was measured by ELISA. Stimulating electrode was inserted into the unilateral nucleus basalis of Meynert (NBM), and repetitive electric stimulation (200μA, 50Hz and 1s on/ 2s off) was performed for 100 minutes. In sham-operated rats, BDNF concentration was stable at a level less than 5pg/ml throughout experiment. In NBM-stimulated rats, BDNF concentration in the cortical perfusate increased significantly at 300-400 minutes after the end of stimulation. The present result suggests that release of BDNF in the cerebral cortex was enhanced by activation of the cholinergic nerve fibers originating in the NBM in the basal forebrain and projecting to the cerebral cortex. The increase in BDNF release in the cerebral cortex is suggested to be partly involved in the protective action of NBM stimulation against ischemia-induced delayed neuronal death that we have reported previously.
|
