scholarly journals Human psychopharmacology and dose-effects of salvinorin A, a kappa opioid agonist hallucinogen present in the plant Salvia divinorum

2011 ◽  
Vol 115 (1-2) ◽  
pp. 150-155 ◽  
Author(s):  
Matthew W. Johnson ◽  
Katherine A. MacLean ◽  
Chad J. Reissig ◽  
Thomas E. Prisinzano ◽  
Roland R. Griffiths
2011 ◽  
Author(s):  
Matthew W. Johnson ◽  
Katherine A. Maclean ◽  
Chad R. Reissig ◽  
Thomas P. Prisinzano ◽  
Roland R. Griffiths

2017 ◽  
Vol 60 (9) ◽  
pp. 3866-3878 ◽  
Author(s):  
Alexander M. Sherwood ◽  
Rachel Saylor Crowley ◽  
Kelly F. Paton ◽  
Andrew Biggerstaff ◽  
Benjamin Neuenswander ◽  
...  

2014 ◽  
Vol 231 (14) ◽  
pp. 2751-2758 ◽  
Author(s):  
Kevin B. Freeman ◽  
Jennifer E. Naylor ◽  
Thomas E. Prisinzano ◽  
William L. Woolverton

1996 ◽  
Vol 270 (2) ◽  
pp. E367-E372 ◽  
Author(s):  
N. F. Rossi ◽  
D. P. Brooks

Although several studies indicate that kappa-opioid agonists induce a water diuresis by inhibiting vasopressin (AVP) secretion, the locus of the kappa-receptors (neurohypophysial vs. hypothalamic) responsible for this effect remains unclear. We have ascertained the effect of the selective kappa-agonist BRL-52656 (BRL) on AVP secretion by using compartmentalized rat hypothalamoneurohypophysial explants in culture. When applied to the hypothalamus, nanomolar concentrations of BRL inhibited osmotically stimulated AVP secretion. This response was blocked by the highly selective kappa-opioid antagonist nor-binaltorphimine (BNI). However, osmotically stimulated AVP release was suppressed at the neurohypophysial site only by 100 nM BRL and was not reversed by BNI but only by naloxone. This dose of BRL, administered to the posterior pituitary compartment, did not appear to act by the agonist gaining access to hypothalamic kappa-opiate receptors, because BNI added to the hypothalamus failed to prevent the inhibition of AVP secretion. The data demonstrate that BRL is a potent inhibitor of osmotically stimulated AVP secretion via activation of kappa-opiate receptors within the hypothalamus, but that higher concentrations of the drug may also stimulate non-kappa-neurohypophysial opiate receptors that suppress AVP release.


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