Therefore, we studied possible changes in excitability, AP waveform and b-AP attenuation as correlates of intrinsic plasticity in MK-2206 2HCl hippocampal CA1 pyramidal cells immediately after a 1�C2 h kainate-induced SE in mice. Our experimental results suggest an acute SE-related modulation of AP dynamics, including reduced somatodendritic excitability and less spread of dendritic excitation. For the experiments juvenile C57BL/6 mice were used with a mean body weight of 10.860.3 g . Status epilepticus was induced by intraperitoneal injection of kainate diluted in a 0.9% NaCl solution . Seizure onset, duration and severity were monitored by video-taping for 3 h . Behavioral observations during this time were scored on a modified Racine-scale from 0 to 7 . According to this scale, stage 0 represents normal BKM120 behavior . Stage 1 was usually followed by stage 2, in which the animals show stretched tail and forelimbs. At stage 3 the animals show various automatisms including repetitive scratching, cycling and head nodding, combined with occasional forelimb cloni, and stage 4 is defined by rearing with continuous forelimb cloni. Finally, stage 5 is defined as rearing and falling, and stage 6 by full motor seizures, sometimes with sudden jumps . All stage transitions due to sudden or gradual changes in behavior during the 3�C4 h post-injection period were plotted against time and the corresponding data points connected by a line . The area under the resultant curve and the number of seizures $ stage 5 served as a measure of SE severity to compare all tested animals of the basic population. Animals which received an i.p. injection of 0.9% NaCl solution without kainate yielded reference data and were not behaviorally analyzed. We have studied the excitability, AP waveform and somatodendritic spread of excitation in hippocampal CA1 pyramidal cells immediately after acute SE in mice, to test for cellular correlates of intrinsic plasticity before or at an early stage of epileptogenesis. Our data suggest that multiple remodeling processes may be active during acute SE. In particular, we observed a reduced excitability, a modulation of the AP waveform and a strengthened attenuation of b-AP-induced dendritic Ca2+ signals. In the absence of direct functional and molecular data on somatodendritic ion channel expression the mechanistic interpretation of our results must remain in part speculative. Our experimental results show that already within a 1�C2 h period after kainate injection excitability parameters of hippocampal CA1 pyramidal cells may be modulated. The observed changes are small on average but may be of pathophysiological relevance. The data support the notion that excitability and spread of dendritic excitation is reduced at this initial time point. Our results are unlikely to reflect a long-lasting form of postictal depression.