ArticleSchizophrenia bulletin2026
Restoring Synaptic Balance in Schizophrenia: Insights From a Thalamo-Cortical Conductance-Based Model.
Article in Schizophrenia bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Predictive coding and neurocomputational psychiatry: a mechanistic framework for understanding mental disorders.Frontiers in psychiatry · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
background and hypothesisThe dysconnectivity hypothesis of schizophrenia suggests that atypical neural communication underlies the disorder's diverse symptoms. Building on this framework, we propose that specific synaptic disturbances within thalamo-cortical circuits contribute to an imbalance in excitation and inhibition, leading to alteration in oscillations. Our study investigates these alterations and explores whether synaptic restoration can remediate neural activity of schizophrenia and align it with healthy patterns. STUDY
designWe analyzed magnetoencephalography data from schizophrenia patients and healthy controls using dynamic causal modeling to identify synaptic differences in thalamo-cortical circuits. The analysis focused on N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), gamma-aminobutyric acid type A (GABA-A), and gamma-aminobutyric acid type B (GABA-B) receptor-mediated connections. In silico synaptic restoration analysis simulated the effects of targeted adjustments to these receptor-mediated connections to assess whether altered neural activity in schizophrenia could be restored to match control patterns. STUDY
resultsSchizophrenia patients showed statistically significant differences in increased NMDA receptor excitation in superficial pyramidal neurons and reduced GABA-B receptor inhibition between interneurons and pyramidal cells. Parameter recovery analysis revealed limitations for these specific parameters, suggesting that receptor-level interpretations should be made with caution. The in silico synaptic restoration analysis indicated that coordinated modifications across multiple synaptic pathways could potentially remediate neural activity to resemble healthy controls.
conclusionsThis restoration approach suggests the complex nature of synaptic dysfunction in schizophrenia may involve coordinated changes across multiple synaptic parameters rather than isolated alterations. While our findings provide preliminary evidence extending the dysconnectivity theory of schizophrenia, the parameter recovery limitations suggest that specific receptor claims should be interpreted with caution.
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