Small conductance Ca(2+)-activated K(+) (SK) channels and voltage-gated A-type Kv4 channels shape dendritic excitatory postsynaptic potentials (EPSPs) in hippocampal CA1 pyramidal neurons. Synaptically evoked Ca(2+) influx through N-methyl-D-aspartate receptors (NMDARs) activates spine SK channels, reducing EPSPs and the associated spine head Ca(2+) transient. However, results using glutamate uncaging implicated Ca(2+) influx through SNX-482-sensitive (SNX-sensitive) Cav2.3 (R-type) Ca(2+) channels as the Ca(2+) source for SK channel activation. The present findings show that, using Schaffer collateral stimulation, the effects of SNX and apamin are not mutually exclusive and SNX increases EPSPs independent of SK channel activity. Dialysis with 1,2-bis(o-aminophenoxy)ethane-N'N'N'-tetraacetic acid (BAPTA), application of 4-Aminopyridine (4-AP), expression of a Kv4.2 dominant negative subunit, and dialysis with a KChIPs antibody occluded the SNX-induced increase of EPSPs. The results suggest two distinct Ca(2+) signaling pathways within dendritic spines that link Ca(2+) influx through NMDARs to SK channels and Ca(2+) influx through R-type Ca(2+) channels to Kv4.2-containing channels.
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