![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 295, Issue 2, 552-562, November 2000
-Opioid Receptors Are More Efficiently Coupled to Adenylyl
Cyclase Than to L-Type Ca2+ Channels in Transfected Rat
Pituitary Cells1
Department of Pharmacology and Toxicology, University of Arkansas
for Medical Sciences, Little Rock, Arkansas (P.L.P); Department of
Pharmacology, The George Washington University, Washington, DC (L.S.,
T.G.H.); Department of Physiology, Cornell University, New York, New
York (E.T.P.); and Department of Pharmacology, University of Minnesota,
Minneapolis, Minnesota (P.Y.L.)
Opioid receptors often couple to multiple effectors within the same
cell. To examine potential mechanisms that contribute to the
specificity by which 
-receptors couple to distinct intracellular effectors, we stably transfected rat pituitary GH3 cells
with cDNAs encoding for -opioid receptors. In cells transfected with a relatively low -receptor density of 0.55 pmol/mg of protein (GH3DOR), activation of -receptors produced inhibition
of adenylyl cyclase activity but was unable to alter L-type
Ca2+ current. In contrast, activation of -receptors in a
clone that contained a higher density of -receptors (2.45 pmol/mg of
protein) and was also coexpressed with µ-opioid receptors
(GH3MORDOR), resulted in not only the expected inhibition
of adenylyl cyclase activity but also produced inhibition of L-type
Ca2+ current. The purpose of the present study was to
determine whether these observations resulted from differences in
-opioid receptor density between clones or interaction between -
and µ-opioid receptors to allow the activation of different G
proteins and signaling to Ca2+ channels. Using the
-opioid receptor alkylating agent SUPERFIT, reduction of available
-opioid receptors in GH3MORDOR cells to a density
similar to that of -opioid receptors in the GH3DOR clone
resulted in abolishment of coupling to Ca2+ channels, but
not to adenylyl cyclase. Furthermore, although significantly greater
amounts of all G proteins were activated by -opioid receptors in
GH3MORDOR cells, -opioid receptor activation in
GH3DOR cells resulted in coupling to the identical pattern of G proteins seen in GH3MORDOR cells. These findings
suggest that different threshold densities of -opioid receptors are
required to activate critical amounts of G proteins needed to produce
coupling to specific effectors and that -opioid receptors couple
more efficiently to adenylyl cyclase than to L-type Ca2+ channels.
This article has been cited by other articles:
|
|
 |
|
  W. Walwyn, S. John, M. Maga, C. J. Evans, and T. G. Hales {delta} Receptors Are Required for Full Inhibitory Coupling of {micro} Receptors to Voltage-Dependent Ca2+ Channels in Dorsal Root Ganglion Neurons Mol. Pharmacol., July 1, 2009; 76(1): 134 - 143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Walwyn, N. T. Maidment, M. Sanders, C. J. Evans, B. L. Kieffer, and T. G. Hales Induction of {delta} Opioid Receptor Function by Up-Regulation of Membrane Receptors in Mouse Primary Afferent Neurons Mol. Pharmacol., December 1, 2005; 68(6): 1688 - 1698. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Shoemaker, B. K. Joseph, M. B. Ruckle, P. R. Mayeux, and P. L. Prather The Endocannabinoid Noladin Ether Acts as a Full Agonist at Human CB2 Cannabinoid Receptors J. Pharmacol. Exp. Ther., August 1, 2005; 314(2): 868 - 875. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. C. Charles, N. Mostovskaya, K. Asas, C. J. Evans, M. L. Dankovich, and T. G. Hales Coexpression of delta -Opioid Receptors with {micro} Receptors in GH3 Cells Changes the Functional Response to {micro} Agonists from Inhibitory to Excitatory Mol. Pharmacol., January 1, 2003; 63(1): 89 - 95. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-G. Liu and P. L. Prather Chronic Agonist Treatment Converts Antagonists into Inverse Agonists at delta -Opioid Receptors J. Pharmacol. Exp. Ther., September 1, 2002; 302(3): 1070 - 1079. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. A. Martin, M. T. Terruso, and P. L. Prather Agonist Activity of the delta -Antagonists TIPP and TIPP-psi in Cellular Models Expressing Endogenous or Transfected delta -Opioid Receptors J. Pharmacol. Exp. Ther., July 1, 2001; 298(1): 240 - 248. [Abstract] [Full Text]
|
|
|
|
|
|
J.-G. Liu and P. L. Prather Chronic Exposure to {micro}-Opioid Agonists Produces Constitutive Activation of {micro}-Opioid Receptors in Direct Proportion to the Efficacy of the Agonist Used for Pretreatment Mol. Pharmacol., July 1, 2001; 60(1): 53 - 62. [Abstract] [Full Text]
|
|
|
|
|
|
N. A. Martin and P. L. Prather Interaction of Co-Expressed {micro}- and {delta}-Opioid Receptors in Transfected Rat Pituitary GH3 Cells Mol. Pharmacol., April 1, 2001; 59(4): 774 - 783. [Abstract] [Full Text]
|
|
|
|
 |
|
 J.-G. Liu, M. B. Ruckle, and P. L. Prather Constitutively Active {micro}-Opioid Receptors Inhibit Adenylyl Cyclase Activity in Intact Cells and Activate G-proteins Differently than the Agonist [D-Ala2,N-MePhe4,Gly-ol5]Enkephalin J. Biol. Chem., October 5, 2001; 276(41): 37779 - 37786. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
