Copy number variation in genes associated with glutamatergic transmission have emerged as significant factor in various mental and neurodegenerative disorders. Recent studies have shed light on the role of the GRIK4 gene, which encodes the GluK4 subunit of kainate receptors, in conditions such as autism and schizophrenia. Specifically, de novo duplications of the GRIK4 have been identified in individuals with autism. Overexpression of the Grik4 gene in a mouse model (GluK4over) leads to social deficits, anxiety and depression and has a significant impact on amygdala neuronal excitability, causing a circuit disequilibrium (Aller et at 2015; Arora et al 2018). To determine the role of particular populations of amygdala neurons in these behavioral abnormalities, we generated a mouse line with extra copies of Grik4, in which the native alleles of the gene were floxed. We then normalized the Grik4 gene dosage specifically in the basolateral amygdala (BLA) by stereotaxically injecting adeno-associated virus (AAV) encoding CRE recombinase and EGFP. Electrophysiological recordings from centrolateral amygdala (CeLA) regular spiking cells and late spiking cells in brain slices revealed that Grik4 dose normalization in BLA resulted in activity normalization in regular but not in late spiking cells. Behavioral experiments showed that this normalization abolished anxiety, depression, and social deficits, but not spatial memory deficits. These findings indicate that regular spiking cells from the CeLA play a vital role in regulating mood disorders, and that modulating their activity could be a potential mechanism for ameliorating anxiety and depression.