The effect of adenosine on the fEPSP was examined in the lateral olfactory tract (Ia input) and associative tract (Ib input) of the rat piriform cortex. The fEPSP evoked in the Ia input showed paired-pulse facilitation, while that in the Ib input showed paired-pulse depression, suggesting a lower resting release probability in the Ia input. This was supported by results showing that MK801 blocked the NMDA receptor-induced fEPSP more rapidly in the Ib input than the Ia input. Adenosine caused dose-dependent inhibition of the fEPSP in both inputs, the sensitivity being higher in the Ib input. This effect was mimicked by the A(1) receptor agonist, CHA, and antagonized by co-application of the A(1) receptor antagonist, DPCPX, showing that adenosine was acting at A(1) receptors. Application of DPCPX alone caused an increase in the fEPSP, the increase being larger in the Ia input. DPCPX also caused paired-pulse depression in both inputs, and the paired-pulse ratio measured in its presence was very similar in both inputs. These results suggest there is a lower endogenous concentration of adenosine in the Ib sublayer than the Ia sublayer, which might account for the native difference in the resting release probability of the two inputs. The adenosine-induced inhibition of the fEPSP in both inputs was associated with a significant reduction in the rate at which MK801 blocked NMDA receptor-mediated fEPSP activity, suggesting a presynaptic location of the A(1) receptors. Blocking of N-, P/Q-type calcium channels occluded the inhibition by adenosine, indicating that they are downstream effectors of presynaptic A(1) receptor activation.