Rodent epilepsy models are widely used to study chronic neuronal dysfunction and brain damage. To elucidate the pathophysiological remodelling at an early stage of an acquired epilepsy we studied acute effects of status epilepticus (SE) induction on action potential waveform and retrograde spread of excitation in CA1 pyramidal cells of the hippocampus. SE was induced by systemic application of kainate (i.p. injection of 30 mg/kg bodyweight) to 3 weeks old C57BL/6 mice, and behavioural manifestation of SE (stage 5 - 6 according to a modified Rancine-scale) was monitored by videotaping for 3 h. Thereafter, the animals were sacrificed, and hippocampal slices where prepared. Individual CA1 pyramidal cells were accessed in the whole-cell patch-clamp configuration and loaded with bis-Fura 2 by diffusion through the patch-pipette. Action potentials were triggered by somatic current injection and action potential backpropagation was monitored with Ca²⁺ imaging techniques at a single excitation wavelength of 395 nm and a 91 Hz sequential frame-rate. In CA1 pyramidal cells from SE mice we observed a pronounced spike broadening associated with a complete loss of the notch typically preceding spike afterdepolarisation (ADP) in sham experiments. Moreover the first spike latency was increased after SE. The suppression of backpropagating action potentials (b-APs) typically seen in sham experiments was further strengthened in CA1 pyramidal cells from SE mice. Our data unveil an acutely reduced dendritic excitability with a likely involvement of a subthreshold activating somatodendritic A-type current (I_SA).