Abstract
Adenylate cyclase supersensitivity represents one possible cellular adaptation associated with chronic opioid action (1). However, the biochemical basis of this phenomenon still remained unclear, since no detectable changes in both the level of stimulatory PGEI receptors and the effector molecule have been reported (2). We, therefore, decided to investigate more closely the role of the stimulatory GTP-binding protein, G s , in neuroblastoma×glioma (NG108-15) hybrid cells following chronic exposure to [D-Ala 2 ,D-Leu 5 ]enkephalin. Although we did not observe any change in the abundance and intrinsic activity of this G protein during the state of opioid tolerance/dependence, we found considerable alterations in the functional interaction of the components comprising the stimulatory axis of adenylate cyclase
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