Abstract
Previous studies have indicated that cocaine binding sites contain both high- and low-affinity binding components and have actions not related to dopamine uptake inhibition. Therefore, it has been studied if concentrations of cocaine in the range of 0.1–100 nM can affect not only dopamine uptake but also the quinpirole-induced inhibition of the K+-evoked [3H]-dopamine efflux from rat striatal synaptosomes. It was found that quinpirole-induced inhibition of K+-evoked [3H]-dopamine efflux was significantly enhanced by cocaine at 1 and 10 nM but not at 0.1 nM with cocaine alone being inactive and 1 nM cocaine lacking effects on [3H]-dopamine uptake in rat striatal synaptosomes. The results indicate the existence of a novel allosteric agonist action of cocaine in low concentrations, not affecting dopamine uptake, at striatal D2 autoreceptors modulating striatal dopamine transmission.
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Acknowledgments
This work was supported by grants from the Swedish Research Council (04X-715), Hjärnfonden (Swedish Brain Foundation) to KF. The authors (L.F.; S.B; T.A.; M.C.T.; S.T.) thank Fondazione Cassa di Risparmio di Ferrara, for financial support.
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Ferraro, L., Beggiato, S., Marcellino, D. et al. Nanomolar concentrations of cocaine enhance D2-like agonist-induced inhibition of the K+-evoked [3H]-dopamine efflux from rat striatal synaptosomes: a novel action of cocaine. J Neural Transm 117, 593–597 (2010). https://doi.org/10.1007/s00702-010-0389-4
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DOI: https://doi.org/10.1007/s00702-010-0389-4