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The tail suspension test (TST) is widely recognized as a useful experimental paradigm for assessing antidepressant activity and depression-like behavior. We have previously identified ubiquitin-specific peptidase 46 ( Usp46 ) as a quantitative trait gene responsible for decreasing immobility time in the TST in mice. This  Usp46  mutation has a 3-bp deletion coding for lysine in the open reading frame, and we indicated that  Usp46  is implicated in the regulation of the GABAergic system. However, it is not known precisely how the immobile behavior is regulated by the GABAergic system. Therefore, in the present study, we examined whether the immobility time is influenced by drugs affecting the action mediated by GABA A  receptor using both 3-bp deleted (the  Usp46  mutant) and null  Usp4 6 ( Usp46  KO) mice. Nitrazepam, an agonist at the benzodiazepine-binding site of the GABA A  receptor, which potentiates the action of GABA, produced a dose-dependent increase in TST immobility time in the  Usp46  mutant mice without affecting general behaviors. The  Usp46  KO mice exhibited short immobility times comparable to the  Usp46  mutant mice, which was also increased by nitrazepam administration. The effects of nitrazepam in the  Usp46  mutant and KO mice were antagonized by flumazenil. These results indicate that the 3-bp deleted  Usp46  mutation causes a loss-of-function phenotype, and that the GABA A  receptor might participate in the regulation of TST immobility time.

Ubiquitin-Specific Peptidase 46 (Usp46) Regulates Mouse Immobile Behavior in the Tail Suspension Test through the GABAergic System