Interaction between synaptic excitation and slow afterhyperpolarization current in rat hippocampal pyramidal cells

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Abstract
1 Whole cell recordings from CA1 pyramidal cells were performed to investigate the interaction between excitatory postsynaptic potentials (EPSPs) or currents (EPSCs), and the slow Ca2+‐dependent K+ current, IsAHP. Blockers of the slow afterhyperpolarization (sAHP) such as isoprenaline (ISO) or noradrenaline (NA) reduced the hyperpolarization that followed a short train of EPSPs, and slowed the decay of summated EPSPs or EPSCs. 2 ISO/NA action on synaptic responses was observed in the absence of action potentials, but was curtailed by Ca2+ chelation (10 mm EGTA in the electrode) and was not observed with a caesium‐based recording solution. This suggests the involvement of an ISO/NA‐sensitive Ca2+‐dependent K+ current without a requirement for regenerative spiking. 3 An ISO/NA‐sensitive sAHP was observed following both NMDA and non‐NMDA receptor‐mediated EPSP trains in nominally zero Mg2+ medium. Isoprenaline sensitivity was blocked by hyperpolarization during EPSPs or by isradipine, suggesting a requirement for voltage‐dependent Ca2+ influx during EPSPs. The data indicate that bursts of EPSPs can activate voltage‐gated Ca2+ channels, which trigger IsAHP during synaptic responses. 4 A decrease in EPSP temporal summation occurred during both spike‐evoked sAHPs and persistent activation of sAHP conductance following internal dialysis with diazo‐2 (2 mm). At constant membrane potential, diazo‐2 caused a decrease in membrane time constant and input resistance and accelerated the rate of EPSP decay. Photolysis of diazo‐2 or application of NA reduced the resting sAHP conductance, causing an increased membrane time constant and input resistance in association with an increase in EPSP half‐width. 5 These results indicate that short bursts of EPSPs can activate a Ca2+‐dependent K+ current resembling IsAHP, and that activation of this current reduces the postsynaptic response to high‐frequency synaptic input. The findings imply that modulation of IsAHP can regulate synaptic efficacy and may influence the threshold for tetanus‐induced synaptic plasticity.