A bibliometric analysis of 710 publications from 2004 to October 2023 reveals growing research interest in psychedelics as treatments for depression. The analysis maps annual publication trends, authorship, countries, institutions, journals, and keywords to visualize emerging frontiers and influential factors. The authors assert that regulation of psychedelic drugs is necessary but should not impede scientific progress.
In a mouse model of depression induced by lipopolysaccharide, CD38 expression increased in the hippocampus and cortex. Pharmacological inhibition or genetic knockout of CD38 reduced neuroinflammation, microglia activation, synaptic defects, and Sirt1/STAT3 signaling, and improved depression-like behaviors. Optogenetic activation of glutamatergic neurons in the hippocampal CA3 region reduced depression susceptibility and lowered CD38 expression. The antidepressant (R)-ketamine suppressed CD38 expression and reversed synaptic defects. Hippocampal CD38 is closely linked to depressive behaviors in this inflammation model, suggesting it as a potential therapeutic target.