长期潜能在内皮和神经元氧化合成酶双重突变的小鼠中减少
1Howard Hughes Medical Institute and Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
Cell
|December 13, 1996
概括
氧化合成酶 (NOS) 在海马长期强化 (LTP) 中发挥作用. 缺乏神经元和内皮NOS的双重突变小鼠在CA1层辐射体中显示LTP降低,表明NOS参与.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 氧化 (NO) 在突触可塑性中的作用是公认的.
- 神经元氧化合成酶 (nNOS) 和内皮氧化合成酶 (eNOS) 对海马长期潜能 (LTP) 的具体贡献仍然不完全理解.
研究的目的:
- 调查关于nNOS和eNOS参与海马体LTP的遗传证据.
- 确定nNOS和eNOS是否可以在LTP中相互补偿.
主要方法:
- 使用了具有nNOS和eNOS向突变的转基因小鼠.
- 在CA1区域的不同层 (辐射层和方向层) 中评估海马的LTP.
主要成果:
- 具有nNOS或eNOS单个突变的小鼠表现出正常的LTP.
- 双重突变小鼠 (nNOS-/eNOS-) 在CA1层辐射体中显著减少了LTP.
- 在CA1层向中的LTP在双重突变小鼠中保持正常.
结论:
- 提供了第一个NOS参与LTP在CA1层辐射体内的遗传证据.
- 在单个突变的小鼠中表明nNOS和eNOS之间的功能补偿.
- 表明在LTP中存在NOS依赖和NOS独立的途径,而层面导向LTP在很大程度上独立于NOS.
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