Curcumin restores rotenone induced depressive-like symptoms in animal model of neurotoxicity: assessment by social interaction test and sucrose preference test.

Environmental toxin rotenone has been associated to with increased Parkinson's disease (PD) prevalence in population. Depression is one of the main non-motor symptoms of PD. Curcumin exhibits neuroprotective action in neurodegenerative diseases. In the study we investigated the effect of pre- and post-treatment of curcumin on rotenone-induced depressive-like behaviors and neurotransmitter alterations in rat model of PD. In pre-treatment phase rats were administered with curcumin (100 mg/kg/day, p.o.) for 2 weeks. After curcumin treatment rotenone (1.5 mg/kg/day, s.c.) was administered in Pre-Cur + Rot group and rotenone alone group for 8 days. Meanwhile, in Post-Cur + Rot group rotenone was injected for 8 days in order to develop PD-like symptoms. After rotenone administration curcumin (100 mg/kg/day, p.o.) was administered in Post-Cur + Rot group for 2 weeks. Depressive-like behaviors were monitored by the forced swim test (FST), open field test (OFT), sucrose preference test (SPT) and social interaction test (SIT). Animals were decapitated after behavioral analysis, striatum and hippocampus were dissected out for neurochemical estimations. Results showed that the rotenone administration significantly (p < 0.01) produced depressive-like symptoms in all depression-related behavioral test. All these behavioral deficits were accompanied by the reduction of striatal and hippocampal neurotransmitter levels following rotenone administration. Pre- and post-treatment with curcumin significantly (p < 0.01) reversed the depressive-like behavior induced by rotenone and significantly (p < 0.01) improved neurotransmitter levels as compared to rotenone injected rats. Our results strongly suggest that normalization of neurotransmitter levels particularly highlights the antidepressant effect of curcumin against rotenone-induced depressive behavior.