Cell Line | Bmax | Kd | Intracellular cAMP Production (% Control) | ||
---|---|---|---|---|---|
DPDPE (1 μM) | TIPP (1 μM) | TIPP-ψ (100 nM) | |||
pmol/mg | nM | ||||
GH3MORDOR | 3.09 ± 0.351-151 | 30.7 ± 0.761-b 1-c | 47.8 ± 1.11-a 1-c | 1-15061.6 ± 0.581-a 1-b | |
GH3DORT-1 | 0.080 ± 0.003 | 0.52 ± 0.23 | 53.7 ± 2.31-c | 59.0 ± 1.21-c | 74 ± 2.81-a 1-b |
GH3DORT-2 | 0.514 ± 0.021 | 0.52 ± 0.12 | 21.3 ± 1.21-b 1-c | 43.3 ± 4.51-b 1-c | 62 ± 2.81-a 1-b |
GH3DORT-8 | 2.16 ± 0.38 | 1.14 ± 0.22 | 22.0 ± 2.31-c | 30.3 ± 1.71-c | 46 ± 2.51-a 1-b |
GH3DORT-9 | 2.25 ± 0.29 | 1.08 ± 0.37 | 19.7 ± 2.01-c | 28.0 ± 2.91-c | 41 ± 5.71-a 1-b |
Saturation binding with [3H]diprenorphine (0.02–5 nM) in GH3MORDOR and GH3 cells containing the tagged δ-opioid receptor (GH3DORT) was used to determine receptor density (Bmax) and affinity (Kd). Nonspecific binding was determined in the presence of 5 μM naloxone. The ability of 1 μM DPDPE, TIPP, or 100 nM TIPP-ψ to inhibit forskolin-stimulated (10 μM) cAMP production was measured as described under Experimental Procedures. Results represent four separate experiments done in triplicate. Data are presented as mean ± S.E.M.
↵1-150 Concentration of 1 μM TIPP-ψ.
↵1-151 Obtained from Martin and Prather, 2001; determined by [3H]DPDPE saturation binding.
↵1-a Statistically different from DPDPE in the same cell line (P < 0.01; Tukey).
↵1-b Statistically different from TIPP in the same cell line (P < 0.01; Tukey).
↵1-c Statistically different from TIPP-ψ in the same cell line (P < 0.01; Tukey).