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首页> 外文期刊>Neuron >Fear Erasure Facilitated by Immature Inhibitory Neuron Transplantation
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Fear Erasure Facilitated by Immature Inhibitory Neuron Transplantation

机译：未成熟的抑制性神经元移植促进恐惧消除

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Transplantation of embryonic g-aminobutyric acid (GABA)ergic neurons has been shown to modify disease phenotypes in rodent models of neurologic and psychiatric disorders. However, whether transplanted interneurons modulate fear memory remains largely unclear. Here, we report that transplantation of embryonic interneurons into the amygdala does not alter host fear memory formation. Yet approximately 2 weeks after transplantation, but not earlier or later, extinction training produces a marked reduction in spontaneous recovery and renewal of fear response. Further analyses reveal that transplanted interneurons robustly form functional synapses with neurons of the host amygdala and exhibit similar developmental maturation in electrophysiological properties as native amygdala interneurons. Importantly, transplanted immature interneurons reduce the expression of perineuronal nets, promote long-term synaptic plasticity, and modulate both excitatory and inhibitory synaptic transmissions of the host circuits. Our findings demonstrate that transplanted immature interneurons modify amygdala circuitry and suggest a previously unknown strategy for the prevention of extinction-resistant pathological fear.
机译：胚胎g-氨基丁酸（GABA）能神经元的移植已被证明可以改变啮齿动物神经和精神疾病模型中的疾病表型。但是，移植的中间神经元是否能调节恐惧记忆仍不清楚。在这里，我们报道胚胎间神经元移植到杏仁核不会改变宿主恐惧记忆形成。移植后大约两周，但不是更早或更晚，灭绝训练会使自发恢复和恐惧反应的恢复明显降低。进一步的分析表明，移植的中间神经元与宿主杏仁核的神经元牢固地形成功能性突触，并在电生理特性方面表现出与天然杏仁核中间神经元相似的发育成熟。重要的是，移植的未成熟神经元减少了神经周神经网络的表达，促进了长期的突触可塑性，并调节了宿主电路的兴奋性和抑制性突触传递。我们的研究结果表明，移植的未成熟中间神经元可改变杏仁核的回路，并提出了以前未知的预防灭绝性病理恐惧的策略。

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