Phospholipase C-related inactive protein type-1 (PRIP-1) modulates inhibitory neurotransmission by regulating the trafficking and phosphorylation of GABA_A receptors in the central nervous system. Dysregulation of GABA_A receptors is known to be responsible for anhedonia, depression and anxiety seen in stress-induced disorder such as major depressive disorder. However, it remains unknown that PRIP-1 has a critical role in anhedonia, depression and anxiety. In the present study, we investigated whether PRIP-1 deficiency affect chronic restraint stress (CRS)-induced behaviors using several anhedonic, depressive- and anxiety-related models (eg, the sucrose preference test for testing anhedonia-like behavior; the forced swim test (FST) for depressive-like behavior; the open field test (OF), the elevated-plus maze test (EPM) and the social interaction test (SI) for anxiety-like behavior). CRS induced a prolonged decrease in sucrose preference in wild-type (WT) mice. Interestingly, PRIP-1 knockout (PRIP-1 KO) mice subjected to CRS exhibited a transient but not prolonged decrease in sucrose preference. In the FST after CRS, PRIP-1 KO mice displayed less immobility than WT mice. In addition, CRS-exposed PRIP-1 KO mice showed a lower level of anxiety-like behavior in the OF, EPM and SI than those WT mice. These results indicate that PRIP-1 KO mice did not exhibit CRS-induced long-lasting anhedonic, depressive- and anxiety-like states. PRIP-1-mediated GABAergic transmission might be involved in the development of stress-induced behavioral changes.