Consistent with this notion, A/N ratios obtained from cocaine/cKD mice were normalized by the stimulation of Rac1 (Fig. 5d and Supplementary Fig. 5e), indicating that heightened activity of Rac1 was sufficient to resume synaptic transmission, potentially by impeding the aberrantly increased trafficking of GluA2-AMPARs in the dendrites of D1-MSNs of cKD mice. This evidence concerns the gene GRIA2 and chronic kidney disease.