| Project/Area Number |
15590073
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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 |
Biological pharmacy
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| Research Institution | Musashino University (2004-2005)
Hoshi University (2003) |
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Principal Investigator |
ABE Kazuho Musashino University, Research Instituite of Pharamaceutical Sciences, Professor, 薬学研究所, 教授 (60202660)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | amygdala / hippocampus / emotion / memory / synaptic plasticity / dementia / 可塑性 / Caシグナル / 長期増強 / Ca^<2+>チャネル / ドパミン / 長期増強(LTP) |
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| Research Abstract |
The number of patients with senile dementia is now increasing. To develop therapeutic drugs for senile dementia, it is necessary to elucidate mechanisms underlying memory formation in the brain. The formation of memory is known to be affected by emotion. Since the amygdala and hippocampus is involved in emotion and memory, respectively, plasticity at amygdalo-hippocampal synapses may underlie the regulation of memory by emotion. In this study, the induction of long-term potentiation (LTP) at basolateral amygdale (BLA)-hippocampal dentate gyrus (DG) was investigated by electrophysiological experiments with anesthetized rats in vivo. The major findings were as follows : 1) the induction of LTP at BLA-DG pathway required the activation of voltage-dependent L-type Ca channels, but not NMDA type of glutamate receptors ; 2) dopaminergic D2 receptors, but not adrenergic beta2 receptors, cholinergic muscarinic receptor and serotonertic receptors, were involved in the induction of LTP at BLA-DG ; 3) Ca2+/calmodulin-dependent protein kinases are required for the induction of LTP at BLA-DG. These findings should give clues for new therapeutic drugs for senile dementia.
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