Pyramidal neuron dendrites express voltage-gated conductances which control synaptic integration and plasticity, but the contribution of the Ca²⁺-activated K⁺-mediated currents to dendritic function is not well understood. Using dendritic and somatic recordings in rat hippocampal CA1 pyramidal neurons in vitro we analyzed the changes induced by the slow Ca²⁺-activated K⁺-mediated after hyperpolarization (sAHP) generated by bursts of action potentials on excitatory postsynaptic potentials (EPSP) evoked at the apical dendrites by Perforant Path-Schaffer collateral stimulation. Both the amplitude and decay time-constant of EPSPs (EPSP) were reduced by the sAHP in somatic recordings. In contrast the dendritic EPSP amplitude remained unchanged, whereas EPSP was reduced. Temporal summation was reduced and spatial summation linearized by the sAHP. The amplitude of the isolated NMDA component of EPSPs (EPSP_NMDA) was reduced, whereas NMDA was unaffected by the sAHP. In contrast the sAHP did not modify the amplitude of the isolated EPSP_AMPA, but reduced AMPA both in dendritic and somatic recordings. These changes are attributable to a conductance increase that acted mainly via a selective shunt of EPSP_NMDA because they were: (i) absent under voltage clamp; (ii) not present with imposed hyperpolarization simulating the sAHP; (iii) missing when the sAHP was inhibited with isoproterenol; and (iv) were reduced under block of EPSP_NMDA. EPSPs generated at the basal dendrites were similarly modified by the sAHP, suggesting both a somatic and apical dendritic location of the sAHP channels. Therefore, the sAHP may play a decisive role in the dendrites by regulating synaptic efficacy and temporal and spatial summation.