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The Kappa Opioid Receptor Agonist 16-Bromo Salvinorin A Has Anti-Cocaine Effects without Significant Effects on Locomotion, Food Reward, Learning and Memory, or Anxiety and Depressive-like Behaviors.

Ross Van de Wetering, Amy W M Ewald, Susan A Welsh, Lindsay Kornberger, Samuel E. Williamson, Bryan D McElroy, Eduardo R Butelman, Thomas E Prisinzano, Bronwyn M Kivell

Molecules June 19, 2023 DOI: 10.3390/molecules28124848 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Preclinical study Peer reviewed
Population Sprague Dawley rats, B6-SJL mice, non-human primates, and HEK-293 cells
Interventions 16-bromo salvinorin A (16-BrSalA) cocaine
Measures elevated plus maze, light-dark test, forced swim test, sucrose self-administration, novel object recognition, progressive ratio schedule
Topics Addiction Anxiety Salvia divinorum
Keywords Animals Humans Mice Rats, sprague-dawley Diterpenes, clerodane Cocaine Receptors, opioid, kappa Reward Locomotion Hek293 cells Side effects Kappa opioid receptor
Key points 16-BrSalA dose-dependently reduced cocaine-primed reinstatement of drug-seeking and cocaine-induced hyperactivity in a kappa opioid receptor-dependent manner, but did not alter progressive-ratio responding for cocaine. It showed fewer side effects than salvinorin A on several behavioral measures, though it still produced conditioned aversion, and it increased dopamine transporter activity and ERK1/2 and p38 signaling.

Abstract

Kappa opioid receptor (KOR) agonists have preclinical antipsychostimulant effects; however, adverse side effects have limited their therapeutic development. In this preclinical study, conducted in Sprague Dawley rats, B6-SJL mice, and non-human primates (NHPs), we evaluated the G-protein-biased analogue of salvinorin A (SalA), 16-bromo salvinorin A (16-BrSalA), for its anticocaine effects, side effects, and activation of cellular signaling pathways. 16-BrSalA dose-dependently decreased the cocaine-primed reinstatement of drug-seeking behavior in a KOR-dependent manner. It also decreased cocaine-induced hyperactivity, but had no effect on responding for cocaine on a progressive ratio schedule. Compared to SalA, 16-BrSalA had an improved side effect profile, with no significant effects in the elevated plus maze, light-dark test, forced swim test, sucrose self-administration, or novel object recognition; however, it did exhibit conditioned aversive effects. 16-BrSalA increased dopamine transporter (DAT) activity in HEK-293 cells coexpressing DAT and KOR, as well as in rat nucleus accumbens and dorsal striatal tissue. 16-BrSalA also increased the early phase activation of extracellular-signal-regulated kinases 1 and 2, as well as p38 in a KOR-dependent manner. In NHPs, 16-BrSalA caused dose-dependent increases in the neuroendocrine biomarker prolactin, similar to other KOR agonists, at doses without robust sedative effects. These findings highlight that G-protein-biased structural analogues of SalA can have improved pharmacokinetic profiles and fewer side effects while maintaining their anticocaine effects.

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