Nutritional and microbiological psychiatry, especially the contribution of the gut microbiota to depression, has become a promising research field over the past several decades. An imbalance in the "microbiota-gut-brain axis", which reflects the constant bidirectional communication between the central nervous system and the gastrointestinal tract, has been used as a hypothesis to interpret the pathogenesis of depression. Alterations in gut microbiota composition could increase the permeability of the gut barrier, activate systemic inflammation and immune responses, regulate the release and efficacy of monoamine neurotransmitters, alter the activity and function of the hypothalamic-pituitary-adrenal (HPA) axis, and modify the abundance of brain-derived neurotrophic factor (BDNF), eventually leading to depression. In this article, we review changes in gut microbiota in depressive states, the association between these changes and depression-like behavior, the potential mechanism linking gut microbiota disruptions and depression, and preliminary attempts at using gut microbiota intervention for the treatment of depression. In summary, although the link between gut microbiota and depression and the potential mechanism have been discussed, a more detailed mechanistic understanding is needed to fully realize the importance of the microbiota-gut-brain axis in depression. Future efforts should aim to determine the potential causative mechanisms, which will require further animal and clinical research as well as the development of analytical approaches.

Quercetin is a polyphenol with multiple biological activities, and results of our preliminary study showed that it could shorten the immobility time of mice in the forced swimming test and tail suspending test. The aim of this study was to investigate its effects on the behavioral performance of lipopolysaccharide (LPS)-challenged rats and explore the potential mechanism. The results showed that intragastrical administration of quercetin (40 mg/kg) could improve the bodyweight gain of LPS-challenged rats, increase the saccharin preference index in the saccharin preference test and the novel arm preference index in the Y-maze, and decrease the immobility time in the FST. However, it showed no significant effect on the performance of LPS-challenged rats in the Morris water maze and the plasma concentrations of nesfatin-1, C-reactive protein (CRP), and IL-6. Results of western blot showed that the expression levels of BDNF, Copine 6, p-TrkB, and the triggering receptors expressed on myeloid cells (TREM) 1 were decreased in both the hippocampus and the prefrontal cortex (PFC) of LPS-challenged rats, while the expression of TREM2 was increased. The protein expression of synapsin-1 was decreased in the hippocampus without significant changes in the PFC. These imbalance protein expressions could be balanced by treatment with quercetin. The results suggested that quercetin could alleviate LPS-induced depression-like behaviors and impairment of learning and memory in rats, the mechanism of which might be involved with regulating the BDNF-related imbalance expression of Copine 6 and TREM1/2 in the hippocampus and the PFC.

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