Upregulated inwardly rectifying K ⁺ current-mediated hypoactivity of parvalbumin interneurons underlies autism-like deficits in <i>Bod1</i>-deficient mice.

ABSTRACT: Parvalbumin-positive (PV ⁺) interneuron dysfunction is believed to be linked to autism spectrum disorder (ASD), a neurodevelopmental disorder characterized by social deficits and stereotypical behaviors. However, the mechanisms behind PV ⁺ interneuron dysfunction remain largely unclear. Here, we found that a deficiency of Biorientation Defective 1 ( Bod1) in PV ⁺ interneurons led to an ASD-like phenotype in Pvalb-Cre; Bod1 ^f/f mice. Mechanistically, we observed that Bod1 deficiency induced hypoactivity of PV ⁺ interneurons and hyperactivity of calcium/calmodulin-dependent protein kinase Ⅱ alpha (CaMKⅡα) neurons in the medial prefrontal cortex, as determined by whole-cell patch-clamp recording. Additio

SUBMITTER: Li C 

PROVIDER: S-EPMC12329414 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature