We compared the effects of the adenosine A1 receptor activation on the postsynaptic potentials (psps) recorded from the CA3 area of immature (postnatal days 10-20) and adult rat hippocampal neurons in vitro. The adenosine A1 receptor agonist 2-phenyl-isopropyl-adenosine (PIA, 1 microM) depressed the stimulus-induced psps less in immature and more in adult neurons. In the presence of the GABAA receptor antagonist bicuculline methiodide (BMI, 10 microM), PIA reduced the duration and number of action potentials of the stimulus-induced paroxysmal depolarizations (PDs) in immature neurons, while it blocked PDs in adult neurons. Spontaneous BMI-induced PDs, were blocked by PIA in less than half (5/12) immature and all (6/6) adult neurons. The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 1 microM) enhanced the stimulus-induced psps in immature and adult neurons alike; this effect did not lead to stimulus-induced bursting in immature neurons. DPCPX induced spontaneous bursts (proconvulsant effect) in only 2/16 immature but in all adult (12/12) neurons. In BMI, DPCPX increased the duration and number of action potentials of the stimulus-induced PDs in immature and adult neurons alike (by about 30%), but it increased the rates of occurrence of spontaneous PDs in significantly more adult neurons. In conclusion, our results suggest that adenosine, acting via A1 receptors, is a more effective endogenous anti-epileptic in adult than in immature hippocampus, a fact which may contribute to the susceptibility of the latter to epileptogenesis.