Skip to content

Peter H. Addy

Johns Hopkins University

2 papers in the library · 106 citations · publishing 2015-2016

Papers

Salvinorin-A Induces Intense Dissociative Effects, Blocking External Sensory Perception and Modulating Interoception and Sense of Body Ownership in Humans

The International Journal of Neuropsychopharmacology June 5, 2015 Marta Valle, Montserrat Puntes, Jimena Coimbra et al. 75 citations

Salvinorin-A, a compound from the plant Salvia divinorum that activates kappa-opioid receptors, produces dose-dependent changes in perception and body awareness. In eight healthy volunteers with prior psychedelic experience, vaporized salvinorin-A at 0.25, 0.50, and 1 mg caused detachment from external reality, elaborate visions, and auditory phenomena. Lower doses increased bodily sensations, while the highest dose produced a complete loss of contact with the body. The effects on body awareness followed an inverted-U pattern, suggesting the kappa-opioid receptor plays a key role in regulating sensory perception, interoception, and the sense of body ownership.

Naltrexone but Not Ketanserin Antagonizes the Subjective, Cardiovascular, and Neuroendocrine Effects of Salvinorin-A in Humans

The International Journal of Neuropsychopharmacology February 12, 2016 Marta Valle, Montserrat Puntes, Jimena Coimbra et al. 31 citations

Salvinorin-A, a terpene from the plant Salvia divinorum, induces an intense but short-lasting altered state of awareness similar to classical psychedelics, but it acts on kappa-opioid receptors rather than serotonin-2A receptors. In a double-blind, placebo-controlled study with 24 healthy volunteers experienced with psychedelics, inhalation of 1 mg of vaporized salvinorin-A severely reduced external sensory perception, caused intense visual and auditory modifications, and increased systolic blood pressure, cortisol, and prolactin. These effects were effectively blocked by the opioid antagonist naltrexone (50 mg orally) but not by the serotonin-2A antagonist ketanserin (40 mg orally), confirming that salvinorin-A's mechanism involves kappa-opioid receptor agonism and not serotonin-2A agonism.