Table 1

δ-Opioid receptor binding and regulation of adenylyl cyclase and calcium channel activity in transfected GH3DOR and GH3MORDOR cells

CloneReceptor BindingAdenylyl Cyclase InhibitionCa2+ Channel Inhibition
BmaxDPDPEKiIC50ImaxIC50Imax
pmol/mg nM % nM %
GH3DOR0.55  ± .071-a 5.8  ± 1.132.2  ± 0.837  ± 2.0No inhibitionNo inhibition
GH3MORDOR2.45  ± .631-b 1.77  ± 0.601.1  ± 0.021-c 78  ± 0.41-c 1.61-d 21  ± 1.31-d

Receptor density (Bmax) values were determined from Scatchard analysis of saturation binding of [3H]diprenorphine (GH3DOR) or [3H]DPDPE (GH3MORDOR). Affinity (Ki) values were determined from competition binding experiments using the same radiolabeled ligands with increasing concentrations of DPDPE (0.01 nM to 10 μM) as described underExperimental Procedures. IC50 and maximal inhibition (Imax) values for δ-opioid receptor inhibition of adenylyl cyclase activity and Ca2+ currents by DPDPE were determined as described under Experimental Procedures. For receptor binding and adenylyl cyclase experiments, data represent the mean ± S.E.M. of a minimum of three separate experiments each performed in triplicate. For electrophysiological experiments, data represent the mean ± S.E.M. of measurements obtained from a minimum of four cells.

  • ↵1-a  Kd = 1.27 ± 0.41 nM.

  • ↵1-b  Kd = 2.32 ± 0.88 nM.

  • ↵1-c  Performed in the presence of 300 nM CTOP.

  • ↵1-d  Obtained from Piros et al. (1996).