Showed that the administration of M084 did not affect locomotor activity of the mice. However, in both FST and TST, M084 caused significant reductions in the immobility time. This gave the first demonstration that M084 might be order BMS-687453 antidepressant, with no effect on the overall spontaneous locomotor activity. Since, anxiety is one of the most common mood disorders associated with depression and several antidepressants, such as fluoxetine and escitalopram, have shown effectiveness in both depression and anxiety disorders , we also tested the possible anxiolytic-like effects of M084 using EPM and L/D tests. In both cases, the administration of M084 increased the exploring activities in the open and illuminated areas, indicative of lowered anxiety. Our findings are in good agreement with the recent studies, which reported that gene ablation of either TRPC4 or TRPC5 decreased anxiety-like behaviors in mice. To further investigate the anti-depression effects of M084, we used the CUS model, which is widely accepted as a mood related disorder animal model that captures core symptoms of depressive disorder. The induction of CUS in mice led to decreased locomotor activity, increased immobility time in FST and prolonged latency to feed in a new environment, indicating the presence of depressed symptoms. The M084 treatment, although did not correct the moderately 103476-89-7 customer reviews reduced locomotor activity, remarkably reversed the CUS-induced increase in immobility time in FST and reduced the latency to feed in NSFT. Previously, it was shown that the latency to feed in NSFT was shortened by chronic, but not acute, treatment of antidepressants. Our finding that an acute single treatment of M084 was beneficial in NSFT following CUS suggests that this new drug is fact acting, which is superior to existing antidepressants in mitigating depression caused by chronic stress. On the other hand, the acute treatment of M084 did not reverse anhedonia, which was also present in mice subjected to CUS. The importance of the BDNF-AKT pathway in anti-depressive treatment has been well-established. Chronic treatment of antidepressants has been shown to increase the expression of BDNF in hippocampus and PFC. Gen
