A single dose of psilocybin given to rats 4–24 hours before a relapse test reduced cue-induced heroin seeking, though it did not alter actual heroin taking. Blocking the serotonin 2A receptor with antagonists worsened relapse. Psilocybin regulated about twice as many genes in the prefrontal cortex at a higher dose, with ketanserin blocking over 90% of these gene changes, including the IL-17a cytokine receptor. Psilocybin also regulated four chemokine/cytokine genes, and selectively inhibiting IL-17a in the prefrontal cortex was enough to reduce heroin relapse. The findings suggest psilocybin reduces heroin relapse and point to IL-17a signaling as a possible downstream pathway.
Psilocybin, a psychedelic compound, causes repetitive, stereotyped movements and reduces defensive reactions in planarian flatworms. These effects are mediated by the neurotransmitter serotonin (5-hydroxytryptamine). The findings suggest that psilocybin's behavioral actions in this simple animal model are linked to serotonergic signaling.
Psilocybin, the active compound in Psilocybe mushrooms, reduced pain-related behaviors in adult male rats exposed to formalin-induced noxious stimuli, a model of both acute and persistent inflammatory pain. Doses of 0.1 and 0.3 mg/kg significantly decreased flinching and licking during both early and late pain phases. Pretreatment with volinanserin, a selective blocker of the 5-HT 2A receptor, eliminated this pain-relieving effect, indicating that psilocybin produces analgesia at least partly by activating that receptor.