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* To whom correspondence should be addressed. E-mail: kumamoto{at}post.saga-med.ac.jp.
The effect of adenosine on inhibitory postsynaptic currents (IPSCs) was examined in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by using the whole-cell patch-clamp technique. Adenosine reversibly reduced the amplitude of GABAergic and glycinergic electrically-evoked IPSCs (eIPSCs) in a dose-dependent manner (EC50 = 14.5 µM and 19.1 µM, respectively). The A1 adenosine-receptor agonist N6-cyclopentyladenosine also reduced the eIPSCs, whereas the A1 antagonist 8-cyclopentyl-1,3-dimethylxanthine reversed the inhibition produced by adenosine. In paired-pulse experiments, the ratio of the second to first GABAergic or glycinergic eIPSC amplitude was increased by adenosine, whereas the response of SG neurons to exogenous GABA or glycine was unaffected. Adenosine reduced the frequency of GABAergic and glycinergic spontaneous IPSCs without changing their amplitude. This reduction in frequency disappeared in the presence of a K+-channel blocker (4-aminopyridine) but not in the absence of Ca2+. The inhibition by adenosine disappeared in the presence of cyclic-AMP analogue (8-Br-cyclic AMP) and adenylate-cyclase activator (forskolin) but not protein-kinase C (PKC) activator (phorbol-12,13-dibutyrate). We conclude that adenosine suppresses inhibitory transmission in SG neurons by activating presynaptic A1 receptors and that this action is mediated by K+ channels and cyclic AMP but not by Ca2+ channels and PKC. This inhibitory action of adenosine probably contributes to the modulation of pain transmission in the SG.
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