Funded by Deanship of Scientific ResearchAmount: 19900 JD
Adenosine has dual functions as a metabolite and as a regulator of cellular processes in most organs. The regulatory functions of adenosine are mediated via four subtypes of G protein-coupled receptors which are distinguished as the A1, A2A, A2B and A3 subtypes (Fredholm et al., 2000). Owing to their widespread occurrence, adenosine receptors have been considered to be important players in pathophysiological situations associated with increased adenosine release and, therefore, are potential targets for drug treatment in numerous diseases. Adenosine is able to influence nociceptive transmission by their functions as extracellular signaling molecules and actions on cell surface receptors. Adenosine acts at several P1 receptors (A1, A2A, A2B, A3), all of which are coupled to G proteins (Fredholm et al., 2000). Activation of adenosine receptors can influence nociception at peripheral, spinal, and supraspinal sites, and affect nociceptive, inflammatory, and neuropathic pain states (Sollevi et al., 1995; Sawynok & Liu, 2003).The role of adenosine A1 receptors (A1Rs) in suppressing pain transmission is prominent, and adenosine receptors as a potential therapeutic target for the treatment of pain, either by directly acting agents (e.g., A1R agonists) or indirectly acting agents that increase endogenous adenosine availability (e.g., adenosine kinase inhibitors), have received considerable recent attention (Kowaluk & Jarvis, 2000; McGaraughty et al., 2005).
Employing both in vivo and in vitro assays, the aim of this study is to investigate the role played by different adenosine receptor on the development of inflammatory pain conditions.