ArticleNeuroscience bulletin2020
Prefrontal Nectin3 Reduction Mediates Adolescent Stress-Induced Deficits of Social Memory, Spatial Working Memory, and Dendritic Structure in Mice.
Article in Neuroscience bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Localization of Puncta Adherentia Junctions at GABAergic Synapses on Parvalbumin-Positive GABAergic Inhibitory Neurons in the Mouse Hippocampus.The Journal of comparative neurology · 2026Article
- New insights into neurodevelopmental disorders by whole genome sequencing of 100 families from Italy.NPJ genomic medicine · 2026Article
- Transdiagnostic and Disorder-Level Genome-Wide Association Studies Enhance Precision of Substance Use and Psychiatric Genetic Risk Profiles in African and European Ancestries.Biological psychiatry · 2026Article
- Adolescent stress exposure induces persistent, sex-specific cognitive deficits.Neurobiology of learning and memory · 2025Article
- Cognitive impairment following maternal separation in rats mediated by the NADTranslational psychiatry · 2025Article
- Dorsal CA1 NECTIN3 Reduction Mediates Early-Life Stress-Induced Object Recognition Memory Deficits in Adolescent Female Mice.Neuroscience bulletin · 2025Article
- Single-nucleus RNA sequencing-based construction of a hippocampal neuron atlas in mice with epileptic cognitive impairment.iScience · 2024Article
- Combining Transdiagnostic and Disorder-Level GWAS Enhances Precision of Psychiatric Genetic Risk Profiles in a Multi-Ancestry Sample.medRxiv : the preprint server for health sciences · 2024Article
- Neuronal Histone Methyltransferase EZH2 Regulates Neuronal Morphogenesis, Synaptic Plasticity, and Cognitive Behavior in Mice.Neuroscience bulletin · 2023Article
- Loss of spines in the prelimbic cortex is detrimental to working memory in mice with early-life adversity.Molecular psychiatry · 2023Article
- CRHR1 antagonist alleviates LPS-induced depression-like behaviour in mice.BMC psychiatry · 2023Article
- Developmental Exposure to Bisphenol a Degrades Auditory Cortical Processing in Rats.Neuroscience bulletin · 2022Article
- Could Alcohol Abuse and Dependence on Junk Foods Inducing Obesity and/or Illicit Drug Use Represent Danger to Liver in Young People with Altered Psychological/Relational Spheres or Emotional Problems?International journal of molecular sciences · 2022Review
- Disrupted presynaptic nectin1-based neuronal adhesion in the entorhinal-hippocampal circuit contributes to early-life stress-induced memory deficits.Translational psychiatry · 2022Article
- Vasopressin Signaling Buffers Synaptic Metaplasticity in a Sex-specific Manner.Neuroscience bulletin · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic stress may disrupt the normal neurodevelopmental trajectory of the adolescent brain (especially the prefrontal cortex) and contribute to the pathophysiology of stress-related mental illnesses, but the underlying molecular mechanisms remain unclear. Here, we investigated how synaptic cell adhesion molecules (e.g., nectin3) are involved in the effects of adolescent chronic stress on mouse medial prefrontal cortex (mPFC). Male C57BL/6N mice were subjected to chronic social instability stress from postnatal days 29 to 77. One week later, the mice exposed to chronic stress exhibited impaired social recognition and spatial working memory, simplified dendritic structure, and reduced spine density in the mPFC. Membrane localization of nectin3 was also altered, and was significantly correlated with behavioral performance. Furthermore, knocking down mPFC nectin3 expression by adeno-associated virus in adolescent mice reproduced the stress-induced changes in behavior and mPFC morphology. These results support the hypothesis that nectin3 is a potential mediator of the effects of adolescent chronic stress on prefrontal structural and functional abnormalities.
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