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.

扬声器响应的经典条件是一种运动学习的一种，并且批判性地取决于小脑。除小脑外，海马还参与了这项运动学习。我们调查了海马在小脑长期抑郁症（LTD） - 缺陷小鼠中的作用，使谷氨酸受体亚基亚基Δ2（GlURΔ2）。这些突变小鼠没有通过CS-US重叠学习延迟的眼神调节，而是在没有CS-US重叠的情况下，学习眼睛闪烁调节，就像野生型小鼠一样成功。接受海马和上覆的皮层抽吸的海马病变的突变小鼠在没有CS-US重叠的眼睛闪烁调节中显示出严重的损害，而对照突变体小鼠接受上层的皮质吸入的控制突变型小鼠没有。与对照野生型小鼠一样成功地学到了海马病变的野生型小鼠。这些结果表明，海马在GLURΔ2突变小鼠中观察到的LTD非依赖性学习机制中起重要作用。

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）。