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<p>Social memory, the ability to recognize and remember conspecifics, is frequently impaired in psychiatric disorders such as autism, yet the underlying mechanisms remain unclear. We examined the role of sleep spindles across non-rapid eye movement sleep in social memory consolidation, focusing on the sensory thalamic reticular nucleus (sTRN). Here we show that impaired spindles were associated with defective social memory. Through pharmacological/optogenetic manipulations and optical Ca<sup>2+</sup> recordings, we demonstrated that parvalbumin-positive neurons in the sTRN (sTRN<sup><i>Pvalb</i></sup>) are essential for sleep spindle generation, mediated by the sTRN<sup><i>Pvalb</i></sup>–ventroposteromedial (VPM) thalamic nucleus circuit. Increasing the activity of the sTRN<sup><i>Pvalb</i></sup>–VPM pathway could rescue impaired spindles and social memory deficits in <i>Neuroligin 2</i> mutant mice. Moreover, we developed machine learning-based models to predict autism in children based on spindle eigenvalues. These findings underscore the critical role of spindles in social memory, suggesting spindles may serve as candidate diagnostic markers.</p>

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Dyscoordination of thalamic reticular spindles is associated with social memory deficits in mice and humans with autism spectrum disorder

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Dongqi Cui,
  • Xiaodan Wang,
  • Ruosong Ai,
  • Feng Gao,
  • Huan Sun,
  • Ying Zhang,
  • Yixuan Lyu,
  • Zhijie Zhang,
  • Wen Li,
  • Yuhang Qin,
  • Yuxi Guo,
  • Yinxia Liu,
  • Ningxia Zhao,
  • Juan Wang,
  • Shen Li,
  • Ying Wu,
  • Siyuan Zhang,
  • Changhe Wang,
  • Feidi Wang,
  • Yan Li

摘要

Social memory, the ability to recognize and remember conspecifics, is frequently impaired in psychiatric disorders such as autism, yet the underlying mechanisms remain unclear. We examined the role of sleep spindles across non-rapid eye movement sleep in social memory consolidation, focusing on the sensory thalamic reticular nucleus (sTRN). Here we show that impaired spindles were associated with defective social memory. Through pharmacological/optogenetic manipulations and optical Ca2+ recordings, we demonstrated that parvalbumin-positive neurons in the sTRN (sTRNPvalb) are essential for sleep spindle generation, mediated by the sTRNPvalb–ventroposteromedial (VPM) thalamic nucleus circuit. Increasing the activity of the sTRNPvalb–VPM pathway could rescue impaired spindles and social memory deficits in Neuroligin 2 mutant mice. Moreover, we developed machine learning-based models to predict autism in children based on spindle eigenvalues. These findings underscore the critical role of spindles in social memory, suggesting spindles may serve as candidate diagnostic markers.