ArticleeNeuro2025
Fxr1 Deletion from Cortical Parvalbumin Interneurons Modifies Their Excitatory Synaptic Responses.
Article in eNeuro, 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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Who cites it
1 citing paper in PubMed.
- Plasma membrane-endoplasmic reticulum coupling probed with genetically-encoded voltage sensors.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Fragile X autosomal homolog 1 (FXR1), a member of the fragile X messenger riboprotein 1 family, has been linked to psychiatric disorders including autism and schizophrenia. Parvalbumin (PV) interneurons play critical roles in cortical processing and have been implicated in FXR1-linked mental illnesses. Targeted deletion of FXR1 from PV interneurons in mice has been shown to alter cortical excitability and elicit schizophrenia-like behavior. This indicates that FXR1 regulates behaviorally relevant electrophysiological functions in PV interneurons. We therefore expressed a genetically encoded hybrid voltage sensor in PV interneurons and used voltage imaging in slices of mouse somatosensory cortex to assess the impact of targeted FXR1 deletion. These experiments showed that PV interneurons lacking FXR1 had excitatory synaptic potentials with larger amplitudes and shorter latencies compared with wild type. Synaptic potential rise-times, decay-times, and half-widths were also impacted to degrees that varied between cortical layer and synaptic input. Thus, FXR1 modulates the responsiveness of PV interneurons to excitatory synaptic inputs. This will enable FXR1 to control cortical processing in subtle ways, with the potential to influence behavior and contribute to psychiatric dysfunction.
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Registered trials
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