Morphine enhances the release of 3H-purines from rat brain cerebral cortical prisms

In vitro experiments have shown that 3H-purines can be released from 3H-adenosine preloaded rat brain cortical prisms by a KCl-evoked depolarization. The KCl-evoked release of 3H-purines is dependent on the concentration of KCl present in the superfusate. At concentrations of 10(-7) approximately 10(-5)M morphine did not influence the basal release of 3H-purines from the prisms, although it enhanced the KCl-evoked release of 3H-purines. The enhancement of KCl-evoked 3H-purine release by morphine was concentration-dependent and was antagonized by naloxone, suggesting the involvement of opiate receptors. Uptake studies with rat brain cerebral cortical synaptosomes show that morphine is a very weak inhibitor of adenosine uptake. Comparisons with dipyridamole, a potent inhibitor of adenosine uptake, suggest that this low level of inhibition of the uptake did not contribute significantly to the release of 3H-purine by morphine seen in our experiments. It is therefore suggested that morphine enhances KCl-evoked 3H-purine release by an interaction with opiate receptors and that the resultant increase in extracellular purine (adenosine) levels may account for some of the actions of morphine.