Trends in Pharmacological Sciences
Adenylate cyclase supersensitivity: a general means of cellular adaptation to inhibitory agonists?
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2010, Biochemical and Biophysical Research CommunicationsCitation Excerpt :One of the biochemical changes during chronic opioid treatment is a significant increase in adenylate cyclase activities stimulated by forskolin or Gs protein-coupled receptor [2,3]. This enhanced responsiveness, known as adenylate cyclase superactivation, eventually counteracts the acute effect of the Gi/o-coupled opioid receptor in inhibiting adenylate cyclase [2–5]. Of three opioid receptor subtypes, μ-opioid receptor (MOR) is the primary target for morphine analgesia.
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2006, NeuroscienceCitation Excerpt :Metabotropic P2Y receptors are coupled to second messenger pathways via either Gq/11 or Gi/o proteins (Filippov et al., 1998; Ralevic and Burnstock, 1998; Torres et al., 2002). In order to establish whether the presynaptic inhibitory action of βγ-imido ATP in mice diaphragm muscles was due to the activation of P2Y receptors coupled to Gi/o proteins, we investigated the effect of PTX (inactivates Gi/o through ADP ribosylation, Gilman, 1984; Thomas and Hoffman, 1987; Watts, 2002) and NEM (uncouple G protein from several receptors, Wu et al., 1992; Shapiro et al., 1994; Yeon et al., 2004). Diaphragms incubated in PTX (2 μM ml−1) for 12–14 h prevented the βγ-imido ATP-mediated reduction in MEPP frequency (12–14 h PTX 101.5±1.9% of control values; 12–14 h PTX+βγ-imido ATP 102.8±1.6%, n=4, Fig. 4A).
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