Abstracts

RATIONALE: Recent studies show that programmed cell death may play a role in seizure-induced neuronal damage. METHODS:_Here, we investigated the spatial and temporal distribution of caspase-3 and caspase-9 immunoreactivities in the rat amygdala and hippocampus after kainic acid-induced status epilepticus. Kainic acid was injected intraperitoneally (9mg/kg) and animals were perfused for histology 1 (n= 4), 2 (n= 4), 4 (n= 4), 8 (n= 3), 16 (n= 5), 24 (n= 4), or 48 (n= 3) hours after kainate injection. Seizure activity was monitored continuously with video-EEG. RESULTS:_In caspase-3 preparations, the density of immunopositive profiles increased at 8 h time point and the maximum was observed at 16-24 h after kainate injection. The highest density of immunoreactive profiles was found in the temporal end of the CA3 and in the dentate gyrus. In the amygdala, most of the immunopositive profiles were located in the periamygdaloid cortex, the anterior and posterior cortical nuclei, the medial nucleus, and the amygdalohippocampal area. In caspase-9 preparations, an increased density of caspase-9 positive elements was detected at 16 hours after kainate injection both in the amygdala and the hippocampus, and the maximum was achieved at 48 h after kainate. In the amygdala, the highest density of immunopositive elements was observed in the anterior and posterior cortical nuclei, the periamygdaloid cortex, and the medial nucleus. In the hippocampus, the most affected regions were the septal and temporal CA1 and the dentate gyrus. CONCLUSIONS:_Our results indicate that the expression of proteases known to mediate programmed cell death increases after status epilepticus in selective regions of the amygdala and the hippocampus. Furthermore, the overexpression of caspases continues far beyond the duration of status epilepticus. ?Supported by Academy of Finland, Sigrid Juselius Foundation and Vaajasalo Foundation??