[Introduction]
Quetiapine is used for the treatment of schizophrenia as an atypical antipsychotic. Although recent study reported that quetiapine may be effective for depressive episode of bipolar disorder, the mechanism underlying the antidepressive potential of quetiapine is currently unknown. In our preliminary study, chronic quetiapine treatment increased hippocampal neurogenesis under non-stress condition. Thus, we hypothesize that quetiapine may exert antidepressive effect through the increase in hippocampal neurogenesis. In this study, we examined whether chronic quetiapine treatment blocks the psychosocial stress-induced reduction of rat hippocampal neurogenesis.
[Methods]
Sprague-Dawley male rats (6 weeks age) were used. Animals were injected intraperitoneally with quetiapine fumarate dissolved in vehicle at a dose of 10 mg/kg once a day for 28 days. Rats were experienced intermittently four times social defeat exposures during the last 2 weeks of drug treatment. At last day of drug treatment, rats were perfused and brains were cut into 40-μm coronal sections throughout the entire hippocampus. A series of tissue (1-in-8 sections) was then processed for doublecortin (DCX) immunostaining and quantified the number of DCX-positive cells in the dentate gyrus.
[Results]
The number of DCX positive cells in dentate gyrus of hippocampus was decreased by psychosocial stress, and increased by quetiapine treatment under non-stress condition. No significant differences between Stress+quetiapine group and Control+vehicle group were found.
[Discussion]
Our findings suggest that chronic quetiapine treatment may block the psychosocial stress-induced reduction of hippocampal neurogenesis in rat.
In future, we need to assess the antidepressive effect of quetiapine treatment on behavioral testing.