Fig. 2. Recovery from hypoxia is impaired when adenosine A1 receptors are blocked with DPCPX. A, Comparison of the time course of the effect of hypoxia on the averaged fEPSP slopes recorded from the CA1 area of hippocampal slices in the absence (control, n = 12) or in the presence (n = 12) of DPCPX, which was perfused for at least 45 min before hypoxia and was kept in the bath up to the end of the experiment; hypoxia was applied as indicated by the horizontal bar. In B and C are shown the statistical comparisons of the fEPSP slopes recorded (as indicated below each column) in control slices (absence of drugs), in slices perfused with DPCPX, and in slices in which, in addition to blocking A1 receptors with DPCPX, adenosine A2Areceptors were also blocked with either SCH 58261 (n = 4) or ZM 241385 (n = 4), the A2A antagonist being applied together with DPCPX and at least 45 min before hypoxia; the results obtained at the end of 80–90 min after starting hypoxia are shown in B, and those obtained at 24–30 min after starting reoxygenation are shown inC. All of the values are mean ± SEM; 100% (averaged fEPSP slopes obtained during 10 min immediately before hypoxia): 0.54 ± 0.04 mV/msec (control), 0.53 ± 0.03 mV/msec (DPCPX), 0.63 ± 0.06 mV/msec (DPCPX plus SCH 58261), and 0.49 ± 0.01 mV/msec (DPCPX plus ZM 241385). *p < 0.05 (one-way repeated-measures ANOVA, followed by the Tukey's multiple comparison test); NS, not statistically significant. Note that the A1 receptor antagonist modified both the hypoxia-induced maximum depression of the fEPSPs and recovery of the fEPSPs, but these were not influenced by additional A2A receptor antagonism.