抄録
A current response induced by adenosine was examined in substantia gelatinosa (SG) neurons by using the whole-cell patch-clamp technique. In 78% of neurons examined, superfusing adenosine induced an outward current at -70 mV in a dose-dependent manner (EC50 = 177 μM). The adenosine current reversed its polarity at a potential which was close to the equilibrium potential for K+ and exhibited a linear current-voltage relationship in a range of -150 to -40 mV. The adenosine current was suppressed by Ba2+ (100 μM) and 4-AP (5 mM) but not by TEA (5 mM). The adenosine current was mimicked by an A1 agonist, CPA (1 μM), and was completely blocked by an A1 antagonist, DPCPX (1 μM). The adenosine current was enhanced in duration by an equilibrative nucleoside-transport (rENT1) inhibitor, S-(4-nitrobenzyl)-6-thioinosine, in a dose-dependent manner in a range of 0.2-5 μM (by 29% at 1 μM) and also by an adenosine-deaminase inhibitor, erythro-9-(2-hydroxy-3-nonyl) adenine (1 μM), by 23%, and slowed in falling phase by an adenosine-kinase inhibitor, iodotubercidine (1 μM). It is concluded in SG neurons that a Ba2+- and 4-AP-sensitive K+ channel exhibiting no rectification is opened through the activation of A1 receptors by adenosine whose level near the receptors is possibly regulated by rENT1, adenosine deaminase and adenosine kinase. This hyperpolarizing action of adenosine might contribute to its antinociceptive effect. [Jpn J Physiol 54 Suppl:S156 (2004)]
