Denholtz L E, Liu J, Nahmoud I, Casaccia P, Likhtik E
Biology Department, Hunter College, CUNY.
Biology Program, The Graduate Center, CUNY.
bioRxiv. 2025 Jul 31:2025.07.25.666881. doi: 10.1101/2025.07.25.666881.
Safety learning is mediated by the infralimbic region (IL) of the medial prefrontal cortex, but its cellular mechanisms are poorly understood. Here we show that safety learning improves cognitive flexibility in the long-term, which is associated with recruitment of oligodendrocyte progenitor cells to a satellite position at parvalbumin (PV) interneurons in the IL and their maturation into oligodendrocytes (OLs), as well as a decrease in perineuronal nets (PNNs) surrounding PVs paired with satellite OLs. Using scRNA transcriptomic data mining, we demonstrate that immature OLs primarily express PNN assembly genes, whereas mature OLs express PNN degradation enzymes. We then demonstrate that inhibiting IL PVs during safety learning prevents safety- induced cognitive flexibility, satellite OL maturation, and PNN degradation around IL PV. Thus, we propose that safety learning drives a novel form of neuroglial plasticity that helps degrade PNNs around PV interneurons via OL recruitment and maturation, thereby shaping IL long-term activity.
安全学习由内侧前额叶皮质的腹内侧前额叶区域(IL)介导,但其细胞机制尚不清楚。在这里,我们表明安全学习能长期提高认知灵活性,这与少突胶质前体细胞募集到IL中小白蛋白(PV)中间神经元的卫星位置并成熟为少突胶质细胞(OLs)有关,同时也与围绕与卫星OLs配对的PVs的神经元周围网(PNNs)减少有关。利用单细胞RNA转录组数据挖掘,我们证明未成熟的OLs主要表达PNN组装基因,而成熟的OLs表达PNN降解酶。然后我们证明在安全学习过程中抑制IL PVs会阻止安全诱导的认知灵活性、卫星OL成熟以及IL PV周围的PNN降解。因此,我们提出安全学习驱动了一种新型的神经胶质可塑性,通过OL募集和成熟来帮助降解PV中间神经元周围的PNN,从而塑造IL的长期活动。