Depression is a disorder of unknown origin and it involves disturbance of many physiological processes. There are many mechanisms in depression including alterations in neurotrophic factors. It has been suggested in this review that an impairment of synaptic plasticity in specific areas of central nervous system, specifically in hippocampus can be an important factor in the pathophysiology of depression. Further, an abnormal neural plasticity may be related to alterations in the level of neurotrophic factors. In context with this, it can be suggested that there can be a connection between occurrences of depression with the disturbance of neurotrophic factors, raising great attention in the recent years. In the present review, it has been tried to explain the significance of insulin-like growth factor in depression by presenting the several important topics such as neurotrophic factors in depression, insulin like growth factor in central nervous system, insulin like growth factor receptor in depression, neurotrophic role of insulin like growth factor and correlation between insulin like growth factor and brain serotonin levels.

A possible association between cholesterol, cholesterol-lowering drug therapy and depression remains an issue of debate. Cholesterol-lowering drugs in general help to control elevated levels of different forms of lipids in patients with hyper-lipidemia. The present review demonstrated that recent research describes the idea that cholesterol can play an important role in governing depression. In this review, several topics such as lipid parameters and central nervous system disorders, lipid parameters and depression, lipid parameters and suicidal attempts, antidepressant effects of cholesterol lowering drugs, cholesterol lowering effects of antidepressants have been discussed. Deepening the studies in this field could be a promising avenue for future research, with implications for treating people with hypercholesterolemia along with depression.

Background: It has been reported that there is an abnormal prostaglandin E levels in depression. Various studies indicated that there has been an elevated levels of prostaglandins (PGs) specifically prostaglandin E (PGE ) in 2 2depression.The objective of the present study was to evaluate the influence of Loxoprofen on immobility Objective: time in absence or presence of Lipopolysaccharide in tail suspension test model of depression in mice. Material and Methods: There was a measurement of immobility time in tail suspension test (TST) in which mice were subjected to the treatment of Loxoprofen (16.8 mg/kg,). The same drug treatment was given 60 min before Lipopolysaccharide p.o.[LPS](0.5 mg/kg, ) and 23 h following LPS separately in mice. There was an evaluation of effect of above i.p. mentioned drugs in locomotor activity of mice.The result of the present study indicated that mice treated with Results: Loxoprofen showed a significant decrease in the immobility time in tail suspension test. LPS-treated mice presented an increase in immobility time when compared to controls 24 h after LPS administration. Similarly, Loxoprofen could only reverse but did not prevent the LPS-induced alterations in the TST. There was no significant effect of Loxoprofen on locomotor activity in mice.The results of the present study indicated that Loxoprofen could influence Conclusion: LPS induced alterations in immobility time in mice in tail suspension test. It also indicated possible anti-depressant effect of Loxoprofen in mice subjected to tail suspension test model of depression, having its possible implication in future treatment of depression.

Objective: The objective of the present study was to evaluate the influence of Loxoprofen in sucrose intake in the absence and presence of Lipopolysaccharide in chronic mild stress model of depression in mice. Methods: There was a measurement of sucrose intake in chronic mild stress model (CMS), consisting of 21 days stress schedule in which mice were subjected to the treatment of Loxoprofen (16.8 mg/kg, p.o.) with or without treatment of lipopolysaccharide (LPS) (0.5 mg/kg i.p.) for the past 14 days. Results: The result of the present study indicated that mice treated with Venlafaxine and Loxoprofen showed a significant increase in the sucrose intake in stressed mice in chronic mild stress model. LPS-treated mice presented a decrease in sucrose intake when compared to controls. Similarly, Venlafaxine and Loxoprofen in the presence of LPS could increase the sucrose intake as compared to LPS treated stressed mice. Conclusion: The results of the present study showed that Loxoprofen could influence LPS induced alterations in sucrose intake in mice in chronic mild stress model. It can also indicate the possible anti-depressant effect of Loxoprofen in mice subjected to chronic mild stress model of depression, having its possible implication in future treatment of depression.

Depression is a chronic syndrome with a pathogenesis linked to various genetic, biological, and environmental factors. Several links between gut microbiota and depression have been established in animal models. In humans, however, few correlations have yet been demonstrated. There is a growing emphasis on the relationship between the complexity and diversity of the microorganisms that inhabit gastrointestinal microbiota and health/disease, including brain health and disorders of the central nervous system. It has been demonstrated that changes in the gut environment can lead to a broad spectrum of physiological and behavioral effects including hypothalamic pituitary adrenal axis activation and altered activity of neurotransmitter systems and immune function. Further, it has been demonstrated that microbiota could be an important in normal healthy brain function. Moreover, the relation between stress and microbiota and how alterations in microbiota influence stress related behaviors has been discussed. It has been demonstrated that bacteria including psychobiotics, probiotics and prebiotics in the gastrointestinal tract could activate neural pathways and central nervous system signaling systems. It is possible that probiotic and prebiotic could affect on emotional, cognitive, systemic and neural variables may be relevant to health and disease. In this review, it has been tried to discuss the role of gut microbiota in brain and depression. It can be concluded from the literature review that utilization of gut microbiota data may provide novel approaches for prevention and treatment of mental illness including depression.