Neuropharmacology
September 1, 2022
Hao-Ming Hua, Chao Huang, Hanyu Liu et al.
35 citations
Ketamine's rapid antidepressant effects, a major advance in depression treatment, may involve the gut-brain axis. This review examines how ketamine and its metabolites interact with the gut microbiome and microbiota-derived molecules. The proposed mechanisms include modulation of the stress response, promotion of brain-derived neurotrophic factor (BDNF)-mediated neurogenesis, anti-inflammatory effects, and regulation of neurotransmitters. However, the exact mechanisms remain unclear.
Translational Psychiatry
September 3, 2021
Chao Huang, Yuanyuan Wang, Zifeng Wu et al.
29 citations
Ketamine acts as a rapid and long-lasting antidepressant, but its molecular mechanisms are unclear. In mice subjected to chronic social stress, microRNA miR-98-5p was downregulated in the prefrontal cortex and hippocampus. Overexpressing miR-98-5p with an agonist alleviated depression-like behaviors. Ketamine administration upregulated miR-98-5p, and inhibiting it with an antagonist blocked ketamine's antidepressant effect. This suggests a novel molecular mechanism for ketamine's action and that targeting miR-98-5p could be beneficial for depression treatment.
Current neuropharmacology
January 16, 2025
Sen Wang, Chaoli Huang, Mengyu Wang et al.
4 citations
Depression affects about 300 million people worldwide, and its underlying mechanisms remain unclear. Changes in oligodendrocytes and myelin are implicated in depression pathology. Conventional antidepressants take weeks to work and fail for about one-third of patients. Ketamine provides rapid, sustained antidepressant effects in treatment-resistant patients. Reduced myelination is linked to depression, so repairing myelin damage may be a key mechanism behind ketamine's prolonged effects. This review summarizes the relationship between demyelination and depression and discusses how ketamine might exert antidepressant effects by repairing myelin, offering new insights into the role of myelination in antidepressant mechanisms.
Neuroscience
March 5, 2025
Hanyu Liu, Siqi Yang, Qi Zhang et al.
Opioid-induced hyperalgesia (OIH) is a complication of pain treatment where opioids paradoxically increase pain sensitivity. Using a mouse model, about 60% of mice developed OIH after three days of morphine, shown by abnormal movement and anxiety-like behaviors. Mice whose gut microbiota were eliminated with antibiotics did not develop hyperalgesia, but those receiving fecal transplants from OIH mice did. S-ketamine, but not R-ketamine, prevented OIH. Gut microbiota analysis revealed increased Enterobacteriaceae in OIH-susceptible mice, which decreased after S-ketamine treatment. The findings suggest S-ketamine alleviates morphine-induced OIH by reducing gut Enterobacteriaceae levels.