Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the appearance (27% of control) and disappearance (15% of control) of TR. Paired pulse studies showed the presynaptic nature of the release of inhibition of synaptic transmission during TR. Both N- and P/Q-type voltage-dependent calcium channels were involved in the appearance of TR. This evidence suggests that underlying mechanisms of TR appearance during hypoxic hypoglycemic insult might be related to ATP depletion and release of A1 adenosine receptor mediated inhibition of presynaptic voltage-dependent calcium channels.