ArticleInvestigative ophthalmology & visual science2026
Cortex-Restricted Deletion of Foxp1 Impairs Visual Responses by Disrupting Geniculocortical Connections in a Mouse Model of Autism.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Visual deficits are prominent features of autism spectrum disorder (ASD), yet the underlying neural mechanisms remain unclear. Mutations in FOXP1, which is a major risk factor for ASD, are often associated with visual issues. This study aims to investigate how the loss of cortical Foxp1 may contribute to the visual problems. Methods: A mouse model of ASD was generated by specific knockout of Foxp1 in cortical progenitors and their descendant excitatory neurons (Foxp1-cKO). We assessed visual depth perception using the visual cliff test. Visual signal conduction was evaluated through flash visual evoked potentials (FVEPs) and light-induced c-Fos neuronal activation in the primary visual cortex (V1). Geniculocortical afferents and connectivity were evaluated by immunolabeling of pre- and post-synaptic markers in V1. Dendrites and spines of layer IV neurons were analyzed using Golgi staining, and mitochondria were examined by Western blots and in neuronal cultures from V1. Results: Foxp1-cKO mice showed deficits in binocular depth perception. The knockout mice exhibited reduced FVEP amplitudes and diminished c-Fos activation in V1 neurons. Knocking out Foxp1 reduced geniculocortical connectivity and decreased dendrites and spines of layer IV neurons of V1. Deletion of Foxp1 impaired the mitochondria in the V1 cortex. Conclusions: Foxp1-cKO mice have deficits in visual signal transmission and depth perception, indicating binocular vision abnormalities. This study highlights the importance of geniculocortical connectivity for binocular vision and offers new insights into the mechanisms underlying ASD-related visual impairments, suggesting future studies to explore therapies aimed at restoring mitochondrial function.
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