Potassium and calcium channel involvement in induction of long-lasting synaptic enhancement by calyculin A, a protein phosphatase inhibitor, in rat hippocampal CA1 region.

In the Schaffer collateral-CA1 pathway in rat hippocampal slices, exposure to calyculin A induced a long-lasting potentiation of the extracellular field potentials with a transient increase in glutamate release. The synaptic enhancement produced by calyculin A was blocked by staurosporine and nicardipine, but not by D,L-2-amino-5-phosphonovalerate. In dissociated CA1 pyramidal cells, calyculin A blocked the action-potential repolarization and fast after-hyperpolarization, and increased spike frequency. These results suggest that calyculin A-induced long-lasting potentiation is triggered by the blockade of Ca(2+)-activated K+ channels, the transient increase of glutamate release and the consequent activation of voltage-gated Ca2+ channels, and is maintained by increases in protein kinases activities.