在缺乏Synapsin I的小鼠中,短暂的突触可塑性发生变化
T W Rosahl1, M Geppert, D Spillane
1Department of Molecular Genetics, Howard Hughes Medical Institute, University of Texas Southwestern Medical School, Dallas 75235.
Cell
|November 19, 1993
概括
突触素I对神经递质释放不至关重要,因为缺乏这种蛋白质的小鼠没有表现出主要的功能缺陷. 然而,它的缺席选择性地增加了配对脉冲促进,这表明它在调节释放方面发挥了作用.
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 遗传学 是一个
背景情况:
- 突触素I是突触囊中的关键蛋白,被认为对神经递质释放至关重要.
- 它在调节突触传输中的确切作用仍然不完全理解.
研究的目的:
- 通过在 synapsin I 基因中产生零突变来研究 synapsin I 对神经递质释放的必要性.
- 在小鼠中描述突触素I缺乏的功能后果.
主要方法:
- 均的重组被用来产生缺陷突触素I (无突变) 的小鼠.
- 进行了电生理学记录,以评估突触传输参数.
主要成果:
- 缺乏突触素I的小鼠在整体幸福感或总体神经系统功能方面没有明显的缺陷.
- 电生理学揭示了一种选择性增加在突触素I-null小鼠的配对脉冲促进.
- 在其他突触参数 (包括长期强化) 中没有发现显著的变化.
结论:
- 突触素I对于神经递质释放的基本过程来说并不必不可少.
- 突触素I可能通过调节刺激后的残留水平来限制过度的神经递质释放.
- 冗余的机制可能会补偿在基本神经传递中失去了突触素I功能.
相关概念视频
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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