Mc. Olianas et al., [Phe(1)Phi(CH2-NH)Gly(2)]nociceptin-(1-13)-NH2 acts as a partial agonist at ORL1 receptor endogenously expressed in mouse N1E-115 neuroblastoma cells, NEUROREPORT, 10(5), 1999, pp. 1127-1131
THE nociceptin derivative [Phe(1)Phi(CH2-NH)Gly(2)]-nociceptin-(1-13)-NH2 (
Phe Phi noc) has been reported to act either as a simple antagonist or as a
full agonist at the opioid receptor-like (ORL1) receptor. In the present s
tudy, we identified the expression of the ORL1 receptor in murine N1E-115 n
euroblastoma cells and used this neuronal system to investigate the pharmac
ological activity of Phe Phi noc. Like nociceptin, Phe Phi noc stimulated t
he binding of [S-35]GTP gamma S (EC50 = 120 nM) and inhibited forskolin-sti
mulated [H-3]cAMP formation (EC50=3.3 nM). However, Phe Phi noc elicited ma
ximal effects lower than those induced by nociceptin, and when combined wit
h nociceptin potently antagonized the responses to the natural agonist (K-i
= 0.9 nM). These data indicate that Phe Phi noc acts as a partial agonist
at the ORL1 receptor endogenously expressed in N1E-115 cells. NeuroReport 1
0:1127-1131 (C) 1999 Lippincott Williams & Wilkins.