Mechanisms of plasticity at amygdalo-hippocampal synapses

杏仁核-海马突触的可塑性机制

• 批准号: 15590073
• 负责人: ABE Kazuho
• 金额: $ 2.3万
• 依托单位: Musashino University (2004-2005)Hoshi University (2003)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2003
• 资助国家: 日本
• 起止时间: 2003 至 2005
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15590073/
• 关键词: 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)

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.

老年痴呆症患者的数量现在正在增加。为了开发治疗老年痴呆症的药物，有必要阐明大脑记忆形成的机制。众所周知，记忆的形成受情绪的影响。由于杏仁核和海马体分别参与情绪和记忆，杏仁核-海马体突触的可塑性可能是情绪调节记忆的基础。本研究以麻醉大鼠为实验对象，通过电生理实验研究了大鼠杏仁基底外侧核(BLA)-海马齿状回(DG)长时程增强(LTP)的诱导。主要结果如下：1)BLA-DG途径LTP的诱导需要激活电压依赖的L型钙通道，而非NMDA型谷氨酸受体；2)多巴胺能D2受体，而不是肾上腺素能β2受体、胆碱能M受体和5-羟色胺受体参与BLA-DG途径LTP的诱导；3)LTP的诱导需要钙/钙调素依赖的蛋白激酶。这些发现应该会为治疗老年痴呆症的新药物提供线索。

项目成果

Involvement of L-type Ca2+ channels in the induction of long-term potentiation in the basolateral amygdale-dentate gyrus pathway of anestherized rats.

L 型 Ca2 通道参与诱导麻醉大鼠基底外侧杏仁核-齿状回通路的长时程增强。

• 发表时间: 2004
• 期刊: Brain Res. 1017(1-2)
• 作者: Y.Niikura;K.Abe;M.Misawa
• 通讯作者: M.Misawa

The induction of long-term potentiation at amygdalo-hippocampal synapses in vivo

• DOI: 10.1248/bpb.26.1560
• 发表时间: 2003-11-01
• 期刊: BIOLOGICAL & PHARMACEUTICAL BULLETIN
• 影响因子: 2
• 作者: Abe, K;Niikura, Y;Misawa, M
• 通讯作者: Misawa, M

Involvement of L-type CaII+ channels in the induction of long-term potentiation in the basolateral amygdale-dentate gyrus pathway of anesthetized rats.

L 型 CaII 通道参与麻醉大鼠基底外侧杏仁核-齿状回通路长时程增强的诱导。

• 发表时间: 2004
• 期刊: Brain Res. 1017(1-2)
• 作者: Y.Niikura;K.Abe;M.Misawa
• 通讯作者: M.Misawa

Involvement of L-type Ca^<2+> channels in the induction of long-term potentiation in the basolateral amygdale-dentate gyrus pathway of anesthetized rats.

L型Ca ^ 2 通道参与麻醉大鼠基底外侧杏仁核-齿状回通路长时程增强的诱导。

• 发表时间: 2004
• 期刊: Brain Research 1017(1-2)
• 作者: Y.Niikura;M.Misawa;K.Abe
• 通讯作者: K.Abe

GABAA receptor-mediated inhibition by ethanol of long-term potentiation in the basolateral amygdale-dentate gyrus pathway in vivo.

GABAA 受体介导的乙醇抑制体内基底外侧杏仁核-齿状回通路的长期增强。

• 发表时间: 2004
• 期刊: Neuroscience 125(1)
• 作者: K.Abe;Y.Niikura;M.Misawa
• 通讯作者: M.Misawa