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Associative Memory Cells of Encoding Fear Signals and Anxiety Are Recruited by Neuroligin-3-mediated Synapse Formation

COMMUNICATIONS BIOLOGY(2024)

Univ Chinese Acad Sci

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Abstract
Acute severe stress may induce fear memory and anxiety. Their mechanisms are expectedly revealed to explore therapeutic strategies. We have investigated the recruitment of associative memory cells that encode stress signals to cause fear memory and anxiety by multidisciplinary approaches. In addition to fear memory and anxiety, the social stress by the resident/intruder paradigm leads to synapse interconnections between somatosensory S1-Tr and auditory cortical neurons in intruder mice. These S1-Tr cortical neurons become to receive convergent synapse innervations newly from the auditory cortex and innately from the thalamus as well as encode the stress signals including battle sound and somatic pain, i.e., associative memory neurons. Neuroligin-3 mRNA knockdown in the S1-Tr cortex precludes the recruitment of associative memory neurons and the onset of fear memory and anxiety. The stress-induced recruitment of associative memory cells in sensory cortices for stress-relevant fear memory and anxiety is based on neuroligin-3-mediated new synapse formation. The social stress caused by a resident/intruder paradigm induces fear memory and anxiety-like behaviors, which rely on the recruitment of associative memory neurons by neuroligin-3-mediated new synapse formation in the sensory cortices.
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要点】:本文揭示了社交压力通过神经连接蛋白-3介导的新突触形成招募编码恐惧信号的联想记忆细胞,从而导致恐惧记忆和焦虑。

方法】:研究采用多学科方法,包括居民/入侵者范式来模拟社交压力,并观察由此产生的突触连接变化。

实验】:通过在S1-Tr皮层中敲低神经连接蛋白-3 mRNA,实验发现这阻止了联想记忆细胞的招募以及恐惧记忆和焦虑的出现。使用的数据集涉及社交压力范式下的小鼠行为和突触连接变化,实验结果显示了神经连接蛋白-3介导的新突触形成对联想记忆细胞招募的重要性。