ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Synaptic Dysfunction in the Anterior Cingulate Cortex Underlies Pain-Anxiety Comorbidity in a Mandibular Asymmetry Mouse Model.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Pain-Affective Disorder Comorbidity in the Temporomandibular Disorders: From Mechanistic Insights to Clinical Management.Neuroscience bulletin · 2026Review
- Electroacupuncture Ameliorates Hyperalgesia and Anxiety-Like Behaviors in Chemotherapy-Induced Peripheral Neuropathy Mice Through Inhibition of Astrocyte-Mediated Neuronal Activation in the Anterior Cingulate Cortex.Journal of pain research · 2026Article
- Synaptic Dysfunction in the Anterior Cingulate Cortex Underlies Pain-Anxiety Comorbidity in a Mandibular Asymmetry Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Structural craniofacial abnormalities, particularly mandibular asymmetry (MA), are increasingly recognized as key drivers of orofacial pain and emotional comorbidities, although the underlying neural mechanisms remain unclear. This study aims to develop a preclinical MA model to investigate the dynamic interplay between craniofacial structural defects and neurobehavioral dysfunction. Longitudinal behavioral phenotyping including von Frey filaments test as well as open field and elevated plus maze tests reveals progressive sensory hypersensitivity and anxiety-like behaviors, with computational ethology revealing subtle but consistent alterations in the naturalistic behaviors. Whole-brain activity mapping reveal hyperactivation in the anterior cingulate cortex (ACC), whereas multi-omics profiling reveal cell type-specific transcriptional changes and synaptic reorganization within this region. Functional investigation including sparse labeling, electrophysiology, western blotting, and chemogenetics demonstrate that the ACC modulation regulated both pain and anxiety. These findings establish a causal association between structural craniofacial defects and maladaptive neural circuit remodeling, with the ACC emerging as a critical therapeutic target. The study provides a comprehensive framework for understanding how anatomical abnormalities translate into persistent neurological dysfunction and offers new avenues for mechanistically informed intervention.
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Registered trials
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