突触素7在高概率的突触中塑造短期可塑性
Delia N Chiu1, Brett C Carter2
1European Neuroscience Institute Göttingen - A Joint Initiative of the University Medical Center Göttingen and the Max Planck Society, 37077 Göttingen, Germany.
概括
在高释放概率突触的短期可塑性是复杂的. 我们发现了两个囊泡释放机制,一个依赖于突触胺7 (Syt7),解释了L4-L2/3突触的异常双相可塑性.
科学领域:
- 神经科学是一个神经科学.
- 细胞神经科学 细胞神经科学
- 突触性可塑性 突触性可塑性
背景情况:
- 高释放概率 (P) 突触通常显示由于囊泡枯竭的短期抑郁.
- 现行模型将短期抑郁归因于释放准备的囊泡后动力潜力 (AP) 的耗尽.
- 在动物体感皮层中的4层到2/3层 (L4-L2/3) 突触表现出非典型的短期可塑性,在短间刺激间隔 (ISI) 没有抑郁.
研究的目的:
- 阐明 L4-L2/3 突触中短期可塑性的双相时间过程背后的机制.
- 研究候选机制,包括神经调节,后突触受体脱敏化和使用依赖的前突触变化.
- 确定Synaptotagmin 7 (Syt7) 在这个突触的短期可塑性中的作用.
主要方法:
- 来自幼年小鼠 (雄性和雌性) 的急性脑切片中的全细胞电生理学.
- 两个光子成像.
- 在不同的刺激间隔 (ISI) 中分析突触传输特性.
主要成果:
- 在单个L4-L2/3突触的释放概率 (P) 根据ISI而异,这解释了观察到的双相短期可塑性.
- 一种依赖突触胺7 (Syt7) 的机制,在短时间的ISI中,有助于短暂增加P.
- 确定了两种不同的囊泡释放过程:一个基本的,快速抑制的机制,缓慢恢复 (τ ≈3秒) 和一个Syt7依赖的促进机制 (τ ≈100毫秒).
结论:
- 在L4-L2/3突触的短期可塑性来自于两个不同的囊泡释放过程的总和.
- Syt7依赖机制在初始AP后暂时增加释放概率,抵消短期ISIs的耗尽.
- 这种双重机制使突触能够在短时间内在多个AP中保持高的神经传递概率.
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