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Taken at face value our data showing stimulation of Ins l, 4, 5 ; P3 formation and inhibition of cAMP turnover suggest that the , t-opioid receptor on SH-SY5Y cells is exhibiting G-protein promiscuity. In a recent report Johnson et al. 1994 ; described in COS cells transiently expressing the cloned opioid receptor , aORl, that promiscuity may occur to cAMP inhibition and inhibition of Ins 1, 4, 5 ; P3 formation. However, our previous studies indicate that both events in SH-SY5Y cells are mediated by a pertussis toxin-sensitive G-protein Smart et al., 1994a ; , implying Gprotein fidelity. Clearly, further studies will be required to settle this issue, using titratable levels of cloned receptors at close to endogenous concentrations. There are two possible mechanisms for the stimulation of Ins 1, 4, 5 ; P3 formation caused bycu-opioids. First y subunits from Gi G. could activate PLC. Alternatively u-opioids could open a Ca2l channel, allowing Ca2 + -influx-dependent activation of PLC. Neither 6-opioid nor a2 agonists stimulated Ins 1, 4, 5 ; P3 formation, while the, -opioid agonist DAMGO did Table 1. ; . It worth noting that SH-SY5Y cells do not express K-opioid receptors Yu et al., 1986 ; . Furthermore, neither 1-opioid nor a2 agonists enhanced the Ins 1, 4, 5 ; P3 response to a submaximal dose of DAMGO, ruling out the possibility that insufficent , y subunits were liberated to have a stimulatory effect. Therefore, as all three of these receptors couple to Gi Yu al., 1986; Lambert and Nahorski, 1990a ; , this indicates that fl y-subunit activation of PLC, as seen in other cell types Birnbaumer, 1992 ; , is unlikely to occur in SH-SY5Y cells. However u- and 8-opioid receptors couple to different subtypes of Gi in SH-SY5Y cells Laugwitz et al., 1993 ; , and they may also couple differentially to Go, as in rat cortical membranes where the two receptor subtypes couple to different types of Go Moriaty et al., 1990; Georgoussi et al., 1993 ; . Thus, as the type of fl y subunit varies between G-protein subtypes Pronin and Gautam, 1992 ; , and some reports indicate that fl y-determined signal transduction is selective Kleuss et al., 1993 ; , there remains the possibility that f y subunits are involved in the stimulatory effects of , u-opioids in SH-SY5Y cells. Fentanyl did not increase Ins 1, 4, 5 ; P3 formation in Ca2 + -free conditions, as previously reported Smart et al., 1994a ; , but subsequent Ca2' replacement at 1 min restored the stimulatory effect. This suggests that, u-opioids may open a Ca2 + channel, and that the subsequent Ca2 + influx activates PLC Cockcroft and Thomas, 1992; Rhee and Choi, 1992 ; . Indeed, it has recently been shown that Ca2 + activates the PLC isoform 81 in transfected Chinese hamster ovary cells Banno et al., 1994 ; . While opioids generally close Ca2 + channels Porzig, 1990 ; , there is evidence that they can also open Ca2 + channels, as seen with &-opioids in NG108-15 cells Jin et al., 1992 ; . Furthermore, K-opioids open Ca2 + channels in both astrocytes and human B cells Heagy et al., 1992; Eriksson et al., 1993 ; . However, this putative opening of Ca2 + channels by , t-opioids was short-lived, with closing oc. Relief of symptoms in patients with irritable bowel syndrome and prozac.

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