成熟ラット脊髄膠様質ニューロンのアデノシン誘起外向き膜電流： シナプス前終末における作用との比較
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Although intrathecal administration of adenosine analogues is known to result in antinociception, cellular mechanisms for this action have not been fully addressed yet. We examined a detail of the actions of adenosine on holding currents, excitatory (glutamatergic) and inhibitory (GABAergic and glycinergic) transmission in substantia gelatinosa (SG) neurons of an adult rat spinal cord slice, and compared their actions in efficacy with each other. Superfusing adenosine (1 mM) induced a current (peak amplitude: 17.6 ± 1.8 pA at -70 mV, n=30) which reversed at a potential being close to the equilibrium potential for K+. K+-channel inhibitors, Ba2+ (100 µM) and 4-aminopyridine (5 mM), reduced the peak amplitude of this current by 65 ± 8% (n=3) and 46 ± 3% (n=3), respectively. An A1 adenosine-receptor agonist, N6-cyclopentyladenosine (CPA, 1 µM), produced a similar outward current having a peak amplitude of 17.6 ± 2.9 pA (n=3) at -70 mV. Adenosine (100 µM) and CPA (1 µM) reduced the peak amplitude of dorsal root-evoked monosynaptic Aδ -fiber EPSCs by 39 ± 5% (n=15) and 50 ± 4% (n=3), respectively. Focally-evoked GABAergic and glycinergic IPSCs in the presence of a non-NMDA receptor antagonist (CNQX) were also reduced in peak amplitude by adenosine [100 µM; by 39 ± 6% (n=6) and 50 ± 7% (n=4), respectively] or CPA [1 µM; by 55 ± 6% (n=3) and 51 ± 17% (n=3), respectively]. All of the adenosine actions were inhibited by an A1 antagonist, 8-cyclopentyl 1,3-dipropylxanthine (1 µM). With respect to efficacies of adenosine, EC50 values for adenosine in inducing outward currents (hyperpolarizations) and reducing monosynaptic Aδ -fiber EPSC, GABAergic and glycinergic IPSC amplitudes were 130, 130, 24 and 21 µM, respectively. It is concluded in SG neurons that adenosine at low doses depresses inhibitory transmission while adenosine at high doses induces hyperpolarization and inhibits excitatory transmission, all of which are due to the activation of A1 receptors. Considering that the SG plays a pivotal role in modulating nociceptive transmission from the periphery, it is suggested that adenosine at low and high concentrations may elicit nociception and antinociception, respectively.
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