Chimeric G Proteins in Fluorimetric Calcium Assays: Experience with Opioid Receptors

Author(s):  
Valeria Camarda ◽  
Girolamo Calo’
Keyword(s):  
2003 ◽  
Vol 308 (2) ◽  
pp. 547-554 ◽  
Author(s):  
Chad M. Thompson ◽  
Heidi Wojno ◽  
Elisabeth Greiner ◽  
Everette L. May ◽  
Kenner C. Rice ◽  
...  

Peptides ◽  
2008 ◽  
Vol 29 (11) ◽  
pp. 1988-1993 ◽  
Author(s):  
Piotr Suder ◽  
Dominika Nawrat ◽  
Adam Bielawski ◽  
Agnieszka Zelek-Molik ◽  
Hana Raoof ◽  
...  

2012 ◽  
Vol 24 (12) ◽  
pp. 2315-2328 ◽  
Author(s):  
Danai-Dionysia Fourla ◽  
Maria-Pagona Papakonstantinou ◽  
Stavroula-Maria Vrana ◽  
Zafiroula Georgoussi

1993 ◽  
Vol 246 (3) ◽  
pp. 233-238 ◽  
Author(s):  
Pao-Luh Tao ◽  
Li-Ren Chang ◽  
Yen-Ping Chou ◽  
Ping-Yee Law ◽  
Horace H. Loh

1993 ◽  
Vol 290 (1) ◽  
pp. 241-247 ◽  
Author(s):  
F Okajima ◽  
H Tomura ◽  
Y Kondo

In an NG 108-15 neuroblastoma x glioma hybrid cell suspension, extracellular ATP (via P2-purinergic receptors) and bradykinin stimulated Ins(1,4,5)P3 formation, which was accompanied by an increase in the cytosolic Ca2+ concentration ([Ca2+]i). Leucine enkephalin (EK) also slightly increased [Ca2+]i in the absence, but not in the presence, of apyrase, which hydrolyses extracellular ATP and ADP to AMP. When the cells were stimulated by P2-agonists or bradykinin prior to the application of EK, EK induces a remarkable rise in [Ca2+]i. This P2-agonist- or bradykinin-assisted EK action was also observed in single cells on a coverslip. A decrease in the extracellular Ca2+ concentration only slightly lowered the EK-induced rise in [Ca2+]i, but treatment of the cells with thapsigargin, an agent which depletes Ca2+ in the Ins(1,4,5)P3-sensitive pool, almost completely abolished EK action. The observed permissive stimulation by EK of Ins(1,4,5)P3 formation induced by a P2-agonist or bradykinin may be a primary event for the EK-induced [Ca2+]i rise. These actions of EK were antagonized by naloxone and completely reversed by prior treatment of the cells with pertussis toxin, whereas the toxin hardly affected the actions of P2-agonists and bradykinin themselves. Thus EK can induce phospholipase C activation and subsequent Ca2+ mobilization, provided that the cells have been previously or are simultaneously stimulated by endogenous adenine nucleotides or by externally applied P2-agonists or bradykinin. In this cross-talk mechanism between opioid receptors and these Ca(2+)-mobilizing agonist receptors, pertussis toxin-sensitive G-proteins play a permissive role.


2002 ◽  
Vol 452 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Javier González-Maeso ◽  
Rafael Rodrı́guez-Puertas ◽  
J.Javier Meana

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