To assess if hypofunction of GluA1-containing AMPARs in excitatory cells of the prefrontal cortex or the hippocampus causes schizophrenia-related deficits, we virally transduced either dorsal PFC (anterior cingulate cortex, ACC, and upper prelimbic cortex, PrL), PrL more exclusively, or the hippocampus of Gria1f/f mice with either GFP-tagged Cre recombinase (Cre groups) or GFP only (control groups) driven by the CamKIIα-promoter, bilaterally (Fig. 1a and Supplementary Fig. 1). The gene discussed is PRL; the disease is schizophrenia.