A single low dose of S-ketamine reduces depression- and anxiety-like behaviors in a rat model of postpartum depression (PPD) created by reproductive hormone withdrawal. The treatment also preserves synaptic plasticity in the hippocampus, as shown by molecular, structural, and electrophysiological measures. The findings suggest that maintaining synaptic plasticity is a key mechanism for S-ketamine's antidepressant effects in this PPD model.
Psilocybin shows therapeutic potential for stress-related neuropsychiatric disorders like depression, anxiety, PTSD, OCD, addiction, and eating disorders, but its mechanisms are complex, involving multiple body systems. This review explores how psilocybin interacts with the gut microbiota, enteric nervous system, and hypothalamic-pituitary axis, influencing bidirectional communication between peripheral and neuronal systems. Understanding these gut-brain interactions could advance psilocybin-based therapies from preparation through long-term integration, potentially extending benefits beyond psychiatric disorders to inflammatory-related conditions.
A single dose of the HCN channel inhibitor DK-AH 269 (cilobradine) produces rapid and sustained antidepressant-like effects in mice subjected to chronic social defeat stress, lasting up to 13 days. The compound reduces pathological HCN-mediated currents and abnormal hyperactivity of dopamine neurons in the ventral tegmental area. Treated mice showed normalized social behavior, restored sucrose preference, and less immobility in the forced swim test compared to vehicle-treated animals. These effects parallel those of a single dose of ketamine, suggesting HCN channels as a novel target for fast-acting, long-lasting antidepressants.