Researchers from Dartmouth University discovered that the antidepressant effects of psilocybin are due to the activation of the serotonin 1B receptor, and not just the 2A receptor, which is responsible for the hallucinogenic effects[4]. Researchers created a new model to study the antidepressant and anxiolytic effects of psilocybin in mice and found that the positive behavioral effects are mediated through the 1B receptor in addition to the 2A receptor[4]. This discovered target molecule could allow the development of modified versions of psilocin that would retain the therapeutic effects without the psychedelic hallucinations[4]. The serotonin system is similar in many species, including mice and humans, with the 1B receptor serving as a target for many migraine medications[4]. A single dose of psilocybin can reduce symptoms of depression and anxiety for several weeks to 6 to 12 months[4]. These findings could overcome significant obstacles to the medical use of psilocybin by allowing its therapeutic benefits without the unwanted psychedelic effects.