Analysis of hippocampal roles in the eyeblink classical conditioning of the mutant mice lacking cerebellar long-term depression.

分析海马在缺乏小脑长期抑郁的突变小鼠眨眼经典条件反射中的作用。

• 批准号: 11680652
• 负责人: KAWAHARA Shigenori
• 金额: $ 2.37万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11680652/
• 关键词: eyeblink; classical conditioning; learning; mouse; cerebellum; hippocampus; long-term depression

The classical conditioning of the eyeblink response is a type of motor learning and critically depends on the cerebellum. In addition to the cerebellum, the hippocampus is also involved in this motor learning. We investigated the role of the hippocampus in the cerebellar long-term depression (LTD)-deficient mice that Jack the glutamate receptor subunit δ2 (GluRδ2). These mutant mice do not learn the delay eyeblink conditioning with CS-US overlap but learn the eyeblink conditioning with no CS-US overlap as successfully as the wild type mice. The hippocampally lesioned mutant mice, receiving aspiration of hippocampus and the overlying cortex, showed a severe impairment in eyeblink conditioning with no CS-US overlap, while the control mutant mice, receiving aspiration of the overlying cortex, did not. The hippocampally lesioned wild type mice learned as successfully as the control wild type mice. These results indicated that the hippocampus plays an important role in the LTD-independent learning mechanism observed in the GluRδ2 mutant mice.

眨眼反应的经典调节是一种运动学习，并且关键取决于小脑。除了小脑之外，海马体也参与这种运动学习。我们研究了海马体在小脑长期抑郁中的作用。 (LTD) 缺陷小鼠，杰克谷氨酸受体亚基 δ2 (GluRδ2) 这些突变小鼠不会学习与 CS-US 重叠的延迟眨眼条件反射。没有CS-US重叠的眨眼条件反射与野生型小鼠一样成功海马损伤的突变小鼠接受海马体和上层皮层的抽吸，在没有CS-US重叠的眨眼条件反射中表现出严重受损，而对照突变体小鼠。接受上层皮层抽吸的小鼠，海马损伤的野生型小鼠的学习效果与对照野生型小鼠一样成功。这些结果表明，海马体在学习过程中发挥着重要作用。在 GluRδ2 突变小鼠中观察到的 LTD 独立学习机制。

项目成果

Kishimoto Y, Kawahara S, Suzuki M, Mori H, Mishina M, Kirino Y: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in delay paradigm but not in trace paradigm."Eur J Neurosci. 13(in press). (2001)

Kishimoto Y、Kawahara S、Suzuki M、Mori H、Mishina M、Kirino Y：“谷氨酸受体亚基 δ2 突变小鼠的经典眨眼调节在延迟范式中受到损害，但在跟踪范式中不受损害。”Eur J Neurosci 13（出版中）。 (2001)

Kishimoto Y: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in delay paradigm but not in trace paradigm."European Journal of Neuroscience. (in press). (2001)

Kishimoto Y：“谷氨酸受体亚基 δ2 突变小鼠的经典眨眼调节在延迟范式中受到损害，但在跟踪范式中不受损害。”《欧洲神经科学杂志》（2001 年出版）。

Kishimoto Y: "Long-trace interval eyeblink conditioning is impaired in mutant mice lacking NMDA receptor subunit ε1."European Journal of Neuroscience. (in press). (2001)

Kishimoto Y：“缺乏 NMDA 受体亚基 ε1 的突变小鼠的长间隔眨眼调节能力受到损害。”《欧洲神经科学杂志》（2001 年出版）。