Proceedings of the National Academy of Sciences of the United States of America
September 3, 2002
Bryan L. Roth, Karen Baner, Richard B Westkaemper et al.
782 citations
Salvinorin A, the active compound in the hallucinogenic plant Salvia divinorum, potently and selectively activates kappa opioid receptors while having no effect on the serotonin 5-HT(2A) receptor targeted by classical hallucinogens like LSD. This makes it the first known naturally occurring nonnitrogenous opioid-receptor subtype-selective agonist. Because Salvinorin A produces perceptual distortions, the findings suggest that kappa opioid receptors play a key role in modulating human perception and that kappa opioid-selective antagonists could be developed as novel treatments for disorders involving perceptual distortions, such as schizophrenia, dementia, and bipolar disorders.
The Journal of pharmacology and experimental therapeutics
March 1, 2004
Charles Chavkin, Sumit Sud, Wenzhen Jin et al.
212 citations
Salvinorin A, a diterpene from Salvia divinorum, is a high-affinity and selective full agonist at human kappa-opioid receptors. In human embryonic kidney-293 cells, salvinorin A fully inhibited forskolin-stimulated cAMP production, while derivatives like 2-propionate and 2-heptanoate were partial agonists. Further tests using chimeric G proteins confirmed its potency and efficacy. In Xenopus oocytes with minimal receptor reserve, salvinorin A acted as a full agonist, more efficacious than standard agonists U50488 and U69593, and similar to dynorphin A. The 2-position substituent is critical for receptor binding and activation. Salvinorin A is the first known naturally occurring non-nitrogenous full agonist at kappa-opioid receptors.
The Journal of pharmacology and experimental therapeutics
August 1, 2006
Michael Ansonoff, Jiwen Zhang, Traci Czyzyk et al.
101 citations
Salvinorin A, the active component of the hallucinogenic plant Salvia divinorum, produces pain relief (antinociception) and lowers body temperature in mice by activating the kappa-opioid receptor. These effects were observed after injection of salvinorin A or a similar compound, salvinorinyl-2-propionate, into the brain of normal mice, but not in mice genetically lacking the kappa-opioid receptor. Salvinorin A showed high affinity specifically for the kappa-1 subclass of opioid receptors. In contrast, salvinorin B, an inactive derivative, had no effect on pain or body temperature. The findings confirm that salvinorin A acts through the kappa-opioid receptor to produce its behavioral effects.
Journal of Natural Medicines
January 1, 2014
Anna P Kowalczuk, Vijayasankar Raman, Ahmed M Galal et al.
13 citations
Salvia divinorum, a species traditionally cultivated in Oaxaca, Mexico, has hallucinogenic properties and is legally controlled in many countries. Proper identification of the plant in fresh and dried forms is important for crime prevention. This paper provides a thorough anatomical description of leaves, petioles, and stems, with detailed investigation and illustration of foliar trichomes. Chromatographic analyses, including TLC and HPLC, were applied to fresh and dried plant material alongside the standard reference salvinorin A. A comprehensive identification method based on anatomical examination combined with chemical analysis is proposed for proper plant recognition.
Neuroscience Letters
December 3, 2008
Pieter Beerepoot, Vincent M Lam, Alice Luu et al.
The kappa opioid receptor agonist salvinorin A, the active compound in Salvia divinorum, can either increase or decrease locomotor sensitization caused by the dopamine agonist quinpirole, depending on dose. Rats received biweekly injections of quinpirole plus salvinorin A (0.04, 0.4, or 2.0 mg/kg) or the synthetic kappa agonist U69593 (0.3 mg/kg) for ten sessions. The highest salvinorin A dose and U69593 both potentiated sensitization; the middle dose had no effect; the lowest dose attenuated it. Structural differences between salvinorin A and U69593 do not affect potentiation, and salvinorin A can bidirectionally modulate dopamine agonist sensitization.