The vulnerability of parvalbumin-expressing interneurons and the associated reduction in inhibitory regulation can disrupt their role in controlling network synchrony as observed in neurological and neuropsychiatric disorders, including epilepsy, schizophrenia, and FXS [192,193,194,195,196,197], especially in the ventral hippocampus [191], contributing to seizure initiation and propagation [179]. This evidence concerns the gene PVALB and fragile X syndrome.