ArticleFrontiers in pharmacology2025
Elevated somatostatin interneuron long-term potentiation minimally regulates temporoammonic plasticity in a mouse model of Fragile X Syndrome.
Article in Frontiers in pharmacology, 2025. 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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1 citing paper in PubMed.
- GABAergic neurons exhibit subtype-specific changes in the developing somatosensory cortex of a rat model of Fragile X Syndrome.Frontiers in neuroscience · 2026Article
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4 authors.
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Abstract
Introduction: Fragile X Syndrome is a common, inherited single gene cause of intellectual disability, associated with autism, epilepsy, anxiety, and sensory disturbances. Many of these features have been attributed to cellular dysfunction leading to impaired synaptic plasticity, in particular through metabotropic glutamate and GABA receptor signalling. The function of these pathways in inhibitory interneurons has not been fully elucidated. In this study we test the hypothesis that somatostatin interneurons (SST-INs) display impaired synaptic plasticity, which leads to circuit-level plasticity deficits. Methods: We use a combination of whole-cell and extracellular recordings in acute hippocampal brain slices prepared from adult, male wild-type and Results: We find that long-term potentiation in SST-INs is enhanced in Discussion: These data show that while SST-IN function is impaired in
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