A, application of ATP (100 μm) caused a reversible inhibition of PF EPSP amplitude. Block of equilibrative transport with 5 μm NBTI and 10 μm dipyridamole caused a reduction in PF EPSP amplitude, which was reversed by block of A1 receptors with 8CPT (1 μm). PF EPSPs were blocked by CNQX at the end of the experiment. Graph plots the amplitude of individual PF EPSPs against time. Inset, application of ATP (*) and NBTI/dipyridamole caused an increase in the paired pulse ratio, confirming a presynaptic site of action. Graph plots the paired pulse ratio against time for the PF EPSPs in A. The average paired pulse ratio for five EPSPs is plotted. B, trace from an ADO biosensor present in the same slice as A. Application of 100 μm ATP caused an increase in adenosine concentration (as a result of metabolism), but 5 μM NBTI/10 μm dipyridamole had no effect. C, trace from an ADO biosensor in a different slice. Application of 5 μm NBTI/10 μm dipyridamole produced a current on the sensor, suggesting an increase in the concentration of purines in the bulk of the slice. D, application of ATP (100 μm) caused a reduction in PF EPSP amplitude, but 5 μm NBTI/10 μm dipyridamole had no effect. There was also no effect on the paired pulse ratio (not illustrated). There is an adenosine tone, as block of A1 receptors with 8CPT (1 μm) increased PF EPSP amplitude. PF EPSPs were blocked by CNQX (10 μm) at the end of the experiment.