Plastic responses in the hippocampus after perforant pathway lesion
| Project/Area Number |
11670928
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
HIZUKAMI Katsuyoshi University of Tsukuba, Department of Psychiatry, Institute of Clinical Medicine, Assisitant Professor, 臨床医学系, 講師 (20229686)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | perforant pathway / hippocampus / giutamate / plasticity / NMDA receptor / ubiquitin / 内嗅領皮質 / Perforant Pathway / NR1サブユニット / NR2A / Bサブユニット |
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| Research Abstract |
Immunohistochemical and immunoblot techniques were employed in order to- clarify the mechanism underlying plastic responses within the hippocampus to perforant pathway lesion.
In the first study in order to clarify the stress response following lesions of the perforant pathway, the alterations in free ubiquitin immunoreactivity was examined in the hippocampus of the rat brain. Immunoreactivity for ubiquitin was remarkably decreased in the cell body and proximal dendrites of neurons throughout the hippocampus at I day post-lesion At 3 days post-lesion, ubiquitin immunoreactivity was recovered in interneurons. At 7 days postlesion ubiquitin immunoreactivity was recovered in pyramidal cells as well as in granule cells. These data suggest that deafferentation of the perforant pathway results in transient reduction in free ubiquitin of the hippocampus, and that the ubiquitin system is involved in hippocampal plasticity following perforant lesions.
In the second study, alterations of NMDAR1 and NMDAR2A/B immunoreactivity after perforant pathway lesion were examined. NMDAR1 was increased in the outer molecular layer at all the time points examined. In contrast although a transient increase in NMDAR2A/B immunolabeling was observed in the outer molecular layer at 3 days post-lesion, no other changes were detectable at any of the time points examined. This study suggests that the loss of perforant pathway fibers results in a compensatory up-regulation of NMDA receptor subunits, and that NMDAR1 might play a more important role in signal transduction through the perforant pathway than does NMDAR2A/B. , ' .
These studies greatly contributed to- elucidate the mechanism underlying plastic responses within the hippocampus to the deafferentation of perforant pathway.
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Report
(4 results)
Research Products
(6 results)
