Adenosine-mediated synaptic depression and EPSP/spike dissociation following high potassium-induced depolarization in rat hippocampal slices.

Simultaneous recordings of orthodromic PS, fEPSP and antidromic PS revealed EPSP/spike (E-S) dissociation, indicating a conversion of input/output relations from early and brief excitability to a late and prolonged depression during the recovery from depolarization induced by high levels of potassium. E-S potentiation was partially attenuated by pre-treating the slices with BAPTA-AM and lidocaine and totally eliminated by a submaximal concentration of muscimol. The time lag for recovery was decreased by the GABA(A) antagonist and completely eliminated by the A(1) antagonist. From these observations, we conclude that Ca(2+) dependent inhibitory suppression is the main cause of a brief period of E-S potentiation, and accumulation of adenosine is the mechanism responsible for prolonged depression of synaptic transmission