Table 1.

NeuroD activity and spine stability influence OPRM1 signaling

	Morphine			Fentanyl
	AC inhibition		Phosphorylated ERK (% of control)	AC inhibition		Phosphorylated ERK (% of control)
	KI (nm)	Maximum inhibition (%)		KI (pm)	Maximum inhibition (%)
PBS	24.2 ± 6.5	30.0 ± 2.7	173 ± 15	165 ± 40	29.2 ± 5.1	178 ± 8
Con-vir	26.0 ± 3.5	28.9 ± 4.2	165 ± 16	201 ± 45	27.4 ± 4.3	174 ± 10
190-vir	67.6 ± 8.1*	10.0 ± 3.1*	125 ± 8*	857 ± 109*	7.7 ± 2.8*	128 ± 4*
190-vir plus nd-vir	38.7 ± 9.4	21.6 ± 3.2	151 ± 5	256 ± 48	23.1 ± 3.8	159 ± 13
nd-vir	22.2 ± 4.8	33.4 ± 2.5	177 ± 25	178 ± 27	27.2 ± 3.1	176 ± 13

Rat primary hippocampal neuron cultures were infected with PBS, con-vir, 190-vir, 190-vir plus nd-vir, or nd-vir for 3 d. Cells were then treated for 5 min with 1 μm morphine or 10 nm fentanyl before ERK phosphorylation was measured. Serial doses of morphine (10 μm∼0.01 nm) or etorphine (100 nm∼0.1 pm) were used to determine the dose response of the agonists to induce adenylyl cyclase (AC) inhibition as described in Materials and Methods. To determine ERK phosphorylation, the immunoreactivity of phosphorylated ERK was normalized to the immunoreactivity of total ERK and β-actin, and the results were further normalized against those in untreated cells. Adenylyl cyclase inhibition induced by agonists was indicated by both IC50 (K_I) and the maximum inhibition. No difference in the basal levels of OPRM1 signaling was observed in different groups.

*Decreased signaling capability of OPRM1.