In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.
In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.
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DOI：
10.1016/j.celrep.2015.10.060
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发表时间：
2015-12-01
期刊：
影响因子：
8.8
通讯作者：
Granato M
中科院分区：
文献类型：
--
作者：
Marsden KC;Granato M
暴露在重复的惊人刺激诱导定居，一种简单的学习形式。尽管它很简单，但重复刺激将强烈的行为反应转化为行为冷漠的精确细胞机制尚不清楚。在这里，我们使用头部限制斑马鱼幼虫监测亚细胞Ca 2+动力学在Mauthner神经元，惊吓命令神经元，在惊吓习惯化在体内。使用Ca 2+报告GCaMP 6s，我们发现，Mauthner神经元侧树突中Ca 2+信号的幅度决定惊吓概率，并且这种树突活性的抑制而不是下游抑制介导了短期习惯化，介导了甘氨酸和N-甲基-D-天冬氨酸（NMDA）受体依赖的短期习惯化。结合起来，我们的研究结果表明，习惯化学习模型中，从前馈抑制性神经元的抑制驱动力增加，结合从听觉传入减少兴奋性输入降低树突和Mauthner神经元的兴奋性。
Exposure to repetitive startling stimuli induces habitation, a simple form of learning. Despite its simplicity, the precise cellular mechanisms by which repeated stimulation converts a robust behavioral response to behavioral indifference are unclear. Here, we use head-restrained zebrafish larvae to monitor subcellular Ca2+ dynamics in Mauthner neurons, the startle command neurons, during startle habituation in vivo. Using the Ca2+ reporter GCaMP6s we find that the amplitude of Ca2+ signals in the lateral dendrite of the Mauthner neuron determines startle probability and that depression of this dendritic activity rather than downstream inhibition mediates short-term habituation mediates glycine and N-methyl-D-aspartate (NMDA) receptor dependent short-term habituation. Combined, our results suggest a model for habituation learning in which increased inhibitory drive from feedforward inhibitory neurons combined with decreased excitatory input from auditory afferents decreases dendritic and Mauthner neuron excitability.