Jamwal Sumit, Islam Rafiad, Kaswan Zoe MacDowell, Ahmed Sahabuddin, Bowers Christian, Giuliano Lauryn, Kaffman Arie
Department of Psychiatry, Yale University School of Medicine, 300 George Street, Suite 901, New Haven CT, 06511, USA.
bioRxiv. 2024 Sep 23:2024.09.21.614236. doi: 10.1101/2024.09.21.614236.
Childhood neglect is associated with cortical thinning, hyperactivity, and deficits in cognitive flexibility that are difficult to reverse later in life. Despite being the most prevalent form of early adversity, little is currently understood about the mechanisms responsible for these neurodevelopmental abnormalities, and no animal models have yet replicated key structural and behavioral features of childhood neglect/deprivation. To address these gaps, we have recently demonstrated that mice exposed to impoverished conditions, specifically limited bedding (LB), exhibit behavioral and structural changes that resemble those observed in adolescents who have experienced severe neglect. Here, we show that LB leads to long-term deficits in reversal learning, which can be fully reversed by briefly exposing LB pups to enrichment (toys) in their home cage from postnatal days 14 to 25. Reversal learning failed to induce normal c-fos activation in the orbitofrontal cortex (OFC) of LB mice, a deficit that was normalized by early enrichment. Additionally, LB decreased the density of parvalbumin-positive cells surrounded by perineuronal nets (PV+PNN+) and increased the ratio of glutamatergic to inhibitory synapse densities in the OFC, deficits that were also reversed by enrichment. Degradation of PNN in the OFC of adult mice impaired reversal learning, reduced c-fos activation, and increased the ratio of glutamatergic to inhibitory synapse densities in the OFC to levels comparable to those observed in LB mice. Collectively, our findings suggest that postnatal deprivation and enrichment impact the formation of PV+PNN+ cells in the OFC, a developmental process that is essential for cognitive flexibility in adulthood.
童年期忽视与大脑皮质变薄、多动以及认知灵活性缺陷有关,这些问题在成年后很难逆转。尽管童年期忽视是早期逆境中最普遍的形式,但目前对于导致这些神经发育异常的机制了解甚少,并且尚无动物模型能够复制童年期忽视/剥夺的关键结构和行为特征。为了填补这些空白,我们最近证明,暴露于贫困环境中的小鼠,特别是有限垫料(LB)环境下的小鼠,会表现出与经历过严重忽视的青少年相似的行为和结构变化。在此,我们表明,LB会导致逆转学习的长期缺陷,而在出生后第14天至25天,将LB幼崽短暂置于丰富环境(有玩具)中饲养,这种缺陷可以完全逆转。逆转学习未能在LB小鼠的眶额皮质(OFC)中诱导正常的c-fos激活,而早期丰富环境可使这一缺陷恢复正常。此外,LB降低了被神经元周围网包围的小白蛋白阳性细胞(PV+PNN+)的密度,并增加了OFC中谷氨酸能突触密度与抑制性突触密度的比值,这些缺陷也可通过丰富环境得到逆转。成年小鼠OFC中神经元周围网的降解会损害逆转学习,降低c-fos激活,并使OFC中谷氨酸能突触密度与抑制性突触密度的比值增加到与LB小鼠相当的水平。总体而言,我们的研究结果表明,出生后剥夺和丰富环境会影响OFC中PV+PNN+细胞的形成,这一发育过程对成年后的认知灵活性至关重要。