κ‐Opioid receptor‐transfected cell lines: modulation of adenylyl cyclase activity following acute and chronic opioid treatments

Avidor‐Reiss, Tomer; Zippel, Renata; Levy, Rivka; Saya, Danielle; Ezra, Vittoria; Barg, Jacob; Matus-Leibovitch, Noa; Vogel, Zvi

doi:10.1016/0014-5793(95)00154-2

Cited by 44 publications

(59 citation statements)

References 18 publications

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“…Our results on AC superactivation after U50,488H pretreatment of the human or rat receptor are similar to those of Avidor-Reiss et al (1995b), who reported that incubation of CHO cells stably transfected with the rat opioid receptor with 1 M U69,593 for 4 h resulted in ϳ250% enhancement of AC activity. In addition, we found that AC superactivation was U50,488H concentration-dependent with an EC 50 value of about 25 nM, which was about 6 times higher than that for stimulation of […”

Section: Discussionsupporting

confidence: 89%

“…Avidor-Reiss et al (1995b) also found that the EC 50 value of U69,593 for inducing AC superactivation was much higher than that for inhibiting AC. We demonstrated U50,488H (1.5 M)-induced AC superactivation was time-dependent, occurring as early as 1 h and with t 1/2 of ϳ2 h. Such a rapid time course suggests that protein synthesis is not required for AC superactivation.…”

Section: Discussionmentioning

confidence: 89%

“…The change was first observed in cultured NG108-15 neuroblastoma ϫ glioma hybrid cells that express the ␦ opioid receptor (Sharma et al, 1975) and later confirmed in several cell systems (for example, Yu et al, 1990;Law et al, 1994;Avidor-Reiss et al, 1995b;Blake et al, 1997a). This phenomenon, referred to as AC superactivation, AC sensitization, or AC supersensitization or cAMP overshoot, has been used as a cellular hallmark of opioid withdrawal.…”

mentioning

confidence: 84%

“…Prolonged treatment of cells stably transfected with the human or rat opioid receptor (hkor or rkor) with U50,488H or U69,593 has been shown to result in AC superactivation (Avidor-Reiss et al, 1995b;Li et al, 2003). It has been previously reported that there are species and agonist differences in agonist-induced regulation of the opioid receptors.…”

mentioning

confidence: 99%

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Differential Effects of Agonists on Adenylyl Cyclase Superactivation Mediated by the κ Opioid Receptors: Adenylyl Cyclase Superactivation Is Independent of Agonist-Induced Phosphorylation, Desensitization, Internalization, and Down-Regulation

Wang

Li²,

Huang³

et al. 2003

J Pharmacol Exp Ther

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Prolonged activation of opioid receptors followed by agonist removal leads to adenylyl cyclase (AC) superactivation. In this study, we examined in CHO cells stably expressing the human or rat opioid receptor (hkor or rkor) whether agonists had differential abilities to induce AC superactivation and whether the hkor and rkor exhibited differential AC superactivation. Pretreatment of the hkor with (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide methanesulfonate (U50,488H) induced AC superactivation in a time-and dose-dependent manner, reaching a plateau at 4 h and 0.1 M. The extents of AC superactivation after a 4-h pretreatment of the hkor with saturating concentrations of agonists were in the order of the full agonists U50,488H, dynorphin A(1-17), (Ϯ)-ethylketocyclazocine, etorphine, and U69,593 Ͼ the high-efficacy partial agonist nalorphine Ͼ the low-efficacy partial agonists nalbuphine, morphine, and pentazocine. Interestingly, the full agonist levorphanol caused much lower AC superactivation than other full agonists and reduced the AC superactivation induced by U50,488H and dynorphin A(1-17) in a dose-dependent manner. The order of relative efficacies of agonists in causing AC superactivation mediated by the rkor was similar to that mediated by the hkor and the extents of AC superactivation were slightly lower. Because the rkor does not undergo U50,488H (1 M)-induced phosphorylation, desensitization, internalization, and down-regulation in these cells, the degree of AC superactivation is independent of these processes. This is among the first reports to demonstrate that relative efficacies of agonists in causing AC superactivation generally correlated with those in activating G proteins and a full agonist reduced AC superactivation induced by another full agonist.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 84%

mentioning

confidence: 99%

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Differential Effects of Agonists on Adenylyl Cyclase Superactivation Mediated by the κ Opioid Receptors: Adenylyl Cyclase Superactivation Is Independent of Agonist-Induced Phosphorylation, Desensitization, Internalization, and Down-Regulation

Wang

Li²,

Huang³

et al. 2003

J Pharmacol Exp Ther

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“…Thus, introduction of GTP-␥-S into cells would activate the entire complement of HEK293 cell G-proteins (Zhou et al, 1995;Zong et al, 1995). Furthermore, we also used somatostatin receptors (Law et al, 1993;Shapiro and Hille, 1993;Reisine and Bell, 1995) and opioid receptors (Shen and Crain, 1994;Avidor-Reiss et al, 1995;Ikeda et al, 1995;Lai et al, 1995;Tallent et al, 1995), both of which can activate a wide variety of G-proteins. Interestingly, all of these manipulations produced robust inhibition of ␣ 1B channels, which had the same ancillary subunit composition as the ␣ 1E channels.…”

Section: Discussionmentioning

confidence: 99%

Selective G-Protein Regulation of Neuronal Calcium Channels

Tóth¹,

Shekter²,

Hui³

et al. 1996

J. Neurosci.

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We examined the properties and regulation of Ca channels resulting from the expression of human ␣ 1B and ␣ 1E subunits stably expressed in HEK293 cells. The ancillary subunits ␤ 1B and ␣ 2 /␦ were also stably expressed in these cell lines. Ca currents in ␣ 1B -expressing cells had the properties of N-type currents. Ca currents in cells expressing ␣ 1E exhibited a novel profile that was similar to the properties of the "R type" Ca current. Introduction of GTP-␥-S into ␣ 1B cells greatly enhanced the extent of prepulse facilitation of the Ca current, whereas it had only a very small effect in ␣ 1E -expressing cells. Activation of somatostatin receptors endogenous to HEK293 cells or opioid receptors, expressed in the cells after transfection, inhibited Ca currents in ␣ 1B -expressing cells. This inhibition was blocked by pertussis toxin and was partially relieved by a depolarizing prepulse. In contrast, no inhibitory effects were noted in cells expressing ␣ 1E channels under the same circumstances. HEK293 cells normally contained G-proteins from all of the four major families. Inhibition of Ca currents by agonists in ␣ 1B -expressing cells was enhanced slightly by the cotransfection of several G-protein ␣ subunits. agonists, however, had no effect in ␣ 1E -containing cells, even after overexpression of different G-protein ␣-subunits. In summary, these results demonstrate that there is a large difference in the susceptibility of ␣ 1B -and ␣ 1E -based Ca channels to regulation by G-proteins. This is so despite the fact that the two types of Ca channels show substantial similarities in their primary sequences.

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Biased Ligands at the Kappa Opioid Receptor: Fine-Tuning Receptor Pharmacology

Brust

2020

Handbook of Experimental Pharmacology

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κ‐Opioid receptor‐transfected cell lines: modulation of adenylyl cyclase activity following acute and chronic opioid treatments

Cited by 44 publications

References 18 publications

Differential Effects of Agonists on Adenylyl Cyclase Superactivation Mediated by the κ Opioid Receptors: Adenylyl Cyclase Superactivation Is Independent of Agonist-Induced Phosphorylation, Desensitization, Internalization, and Down-Regulation

Differential Effects of Agonists on Adenylyl Cyclase Superactivation Mediated by the κ Opioid Receptors: Adenylyl Cyclase Superactivation Is Independent of Agonist-Induced Phosphorylation, Desensitization, Internalization, and Down-Regulation

Selective G-Protein Regulation of Neuronal Calcium Channels

Biased Ligands at the Kappa Opioid Receptor: Fine-Tuning Receptor Pharmacology

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