Psilocybin restores deficits in the metabotropic glutamate receptor 2 (mGluR2) caused by alcohol, which leads to the reversal of pathological behaviors associated with alcoholism.
Psilocin, the psychoactive metabolite of psilocybin, triggers a cascade of neuroplastic changes in human cortical neurons derived from stem cells. It reduces cell-surface 5-HT2A receptors, increases BDNF abundance, alters gene expression toward plasticity, enhances neuronal complexity and synaptic protein levels, and boosts excitability and network activity. These findings suggest psilocin induces a state of enhanced neuronal plasticity that may underlie its therapeutic effects in neuropsychiatric disorders involving synaptic dysfunction.
Psilocin, the psychoactive metabolite of psilocybin, increases BDNF abundance in human cortical neurons derived from induced pluripotent stem cells via the 5-HT2A receptor. Transcriptomic profiling shows gene expression changes that prime neurons for neuroplasticity. Morphologically, psilocin enhances neuronal complexity and increases synaptic proteins, especially in the postsynaptic compartment. Functionally, it leads to increased excitability and enhanced synaptic network activity. These findings suggest psilocin induces a state of enhanced neuronal plasticity, which may explain its therapeutic potential in neuropsychiatric disorders involving synaptic dysfunction.