Psilocybin therapy for depression shows promise, but its causal mechanisms are unknown. By comparing brain dynamics in treatment responders (those with >50% symptom reduction) and non-responders before treatment, researchers used large-scale brain modeling to identify brain regions whose perturbation could shift a depressive brain state to a healthy one. The identified regions correlated with density maps of serotonin receptors 5-HT2a and 5-HT1a, where psilocin (psilocybin's active metabolite) acts as an agonist. These findings provide causal mechanistic evidence linking specific brain regions and serotonergic transmission to recovery from depression via psilocybin.
Psilocybin therapy for depression shows promise, but how it works is unclear. By comparing responders (those with >50% reduction in symptoms) to non-responders after 10mg and 25mg doses, whole-brain modeling identified specific brain regions whose dynamics shift from a depressive to a healthy state. These regions overlap with maps of serotonin 5-HT2A and 5-HT1A receptors, which psilocin—the active metabolite of psilocybin—activates. The findings provide causal evidence linking serotonergic transmission and recovery from depression via psilocybin.
Normal waking consciousness requires a balance between global integration (long-distance brain interactions) and segregation (local processing). Altered states, such as anesthesia, tip this balance. Using electrocorticography (ECoG) in a monkey under ketamine or propofol anesthesia, the study examined band-specific synchronization across the whole brain and within localized clusters. Both anesthetics caused a loss of long-range integration in multiple frequency bands, most pronounced in beta (13-30 Hz) and low-gamma (30-80 Hz) bands, while local synchrony was strongly preserved in all bands. This demonstrates a shift away from the integration/segregation equilibrium at sub-second time scales.