Researchers used two-photon microscopy to track individual dendritic spines - the small structures through which neurons connect - in living mice after psilocybin. Within a day, the drug increased spine formation and sped the development of new spines into larger, more stable, receptor-rich connections that lasted for weeks. Its effects varied with the brain’s condition: in healthy mice, new spine growth occurred alongside the pruning of older connections, while in mice exposed to chronic stress, psilocybin produced a larger increase in new spines and prevented the continued loss of existing synapses. The findings suggest that the drug reshapes circuits rather than simply increasing connectivity across the board.
The researchers also tested whether this structural remodeling requires the psychedelic experience. By changing serotonin 2A receptor activity in cortical layer 5 pyramidal neurons, they found that these receptors were necessary and sufficient for psilocybin-induced synaptic changes, but not for the head-twitch response used as a rodent proxy for hallucinations. Conversely, that behavior could occur without the synaptic remodeling. This separation points to distinct pathways for plasticity and psychedelic effects, and offers a rationale for developing compounds that promote neural repair without hallucinogenic effects. The experiments were conducted in mice, so they identify mechanisms relevant to depression research rather than demonstrating that psilocybin replaces lost synapses in people.
Summary generated by AI from the linked article. hn.today is not affiliated with Hacker News or Y Combinator.
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