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在自闭症模型中,核内中加速的社会代表性漂移
Pingping Zhao1, Xing Chen1, Arash Bellafard1
1Department of Neurology, David Geffen School of Medicine, University of California; Los Angeles, Los Angeles, CA, USA.
bioRxiv : the preprint server for biology
|August 14, 2023
概括
社交互动由核 (NAc) 神经元编码,但这种代码在自闭症谱系障碍 (ASD) 中被降解. 抑制特定的NAc神经元在ASD小鼠模型中改善了社会行为.
科学领域:
- 神经科学是一个神经科学.
- 自闭症谱系障碍研究研究
- 奖励回路是一个奖励回路.
背景情况:
- 社交互动缺陷是自闭症谱系障碍 (ASD) 的标志,可能源于改变的奖励处理.
- 核心聚合体 (NAc) 是大脑奖励系统的关键组成部分,在社会行为中发挥作用,但其在ASD中的特定编码机制尚不清楚.
研究的目的:
- 研究NAc神经元组合如何编码社会相互作用.
- 确定这些社会表征是否在ASD小鼠模型中发生变化.
主要方法:
- 使用微型显微镜进行成像,以识别NAc组合.
- 记录NAc群体活动,特别是表达D1受体的中状神经元 (D1-MSN).
- 利用光遗传学来操纵Cntnap2-/-小鼠中的NAc神经活动 (一种ASD模型).
主要成果:
- 纳克人口活动,特别是D1-MSN活动,预测了社会相互作用时代.
- 在NAc中确定了社会相互作用的稳定群体代码,但在Cntnap2-/-小鼠中显著降解.
- 非特定的NAc核心抑制改善了Cntnap2-/-小鼠的社交互动和社交能力.
- 观察到D1-MSN (抑制减少相互作用) 和D2-MSN (抑制增加相互作用) 抑制的不同影响.
结论:
- 社会互动是由NAc神经元优先,具体和动态编码的.
- 在NAc中社会表征的退化是这种ASD小鼠模型的一个关键特征.
- 调节NAc的神经活动为改善ASD社会缺陷提供了潜在的治疗途径.
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