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谷氨酸脱糖酶异型的前突触性贩运对于基底GABAergic神经传递是不可或缺的
Orion Benner1, Charles H Karr1, Thomas M Bartol2
1Biochemistry & Molecular Biology, Colorado State University, Fort Collins, CO 80523, USA.
概括
谷氨酸脱碳酶 (GAD) 酶 GAD65 和 GAD67 产生 γ-氨基黄油酸 (GABA). 它们的位置不会影响GABA的产生;扩散确保了足够的GABA用于突触传输.
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
- 生物化学 生物化学
背景情况:
- 两个主要的谷氨酸脱碳酶 (GAD) 异型,GAD65和GAD67,在神经系统中合成大部分γ-氨基黄油酸 (GABA).
- GAD65和GAD67对突触GABA释放的亚细胞分布和相对影响尚不清楚.
- 了解GAD局部化对于理解GABAergic神经传递调节至关重要.
研究的目的:
- 研究GAD65和GAD67在小鼠大脑和神经元培养中的突触贩运.
- 为了确定亚细胞局部化是否影响GABA的产生和释放.
- 评估功能冗余性和需要在GABAergic传输中招募突触前GAD.
主要方法:
- 在雄性和雌性小鼠大脑和解离的神经元培养中监测GAD65和GAD67的突触贩运.
- 在来自男性干细胞系的缺少GAD的人类神经元中单独表达GAD异型.
- 从GAD异型体中交换或删除贩运信号,并将其局部化限制在非突触区.
主要成果:
- 两种GAD65和GAD67都在GABAergic前突触中富含,与其他谷氨酸生物合成酶不同.
- 当单独表达时,GAD65显示出比GAD67更优越的前突触分布.
- 尽管局部差异,但两种GAD都产生了相当的GABA水平,突变变异型仍然支持GABAergic传播,表明功能冗余.
结论:
- 当均等表达时,GAD65和GAD67在GABA生产中是功能冗余的.
- GADs的亚细胞贩运不会严重影响GABAergic传播.
- 从遥远的细胞内来源扩散GABA有效地为神经传递提供了突触前终端.
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