Abstracts

Rationale: Status epilepticus(SE) may increase neuronal energy demands in the epileptogenic area and energy dements may increase entire cerebral region, including the splenium. However, the mechanism responsible for the lesion in the splenium is poorly understood. The present study was conducted to provide evidence as to whether AQP 4 has different expression on the splenium during and after pilocarpine-induced status epileptic rat compared with normal control rat. Methods: Sprague Dawley (SD) rats (9 11 weeks old) were treated with LiCl (127 mg/kg, intraperitoneally 20 hours before the pilocarpine treatment. Animals were treated with pilocarpine (25 mg/kg, i.p.) 30 minutes after scopolamine butylbromide (2 mg/kg, i.p.). Diazepam pretreatment completely prevented SE. Diazepam-pretreated animals were used as controls at designated time courses (1 day, 2 days, 1 week, and 4 weeks after SE, n = 5). Tissue Processing and Immunohistochemistry: The tissues were incubated in rabbit anti-AQP4 antibody and then incubated sequentially in goat anti-rabbit-pig IgG. Statistical analysis: All data obtained from image analysis were analyzed using one-way ANOVA test to determine statistical significance. Bonferroni s test was used for post hoc comparisons. A P value below either 0.01 or 0.05 was considered statistically significant. Results: In non-SE animals, AQP4 immunoreactivity was weakly detected in the corpus callosum, except in the splenium. Therefore, AQP4 immunoreactivity in the splenium was significantly higher than that in other regions (p < 0.05). Following SE, AQP4 immunoreactivity was significantly elevated in the corpus callosum compared to non-SE animals (p < 0.05). The increase in AQP4 immunoreactivity was peaked at 2 days after SE. However, there was no difference in AQP4 immunoreactivity among the regions of corpus callosum. Conclusions: Our result shows that AQP 4 is elevated in the pilocarpine-induced SE rat. These results suggest that cytotoxic edema on the splenium is related with AQP 4 change. AQP4 is expressed in astrocyte foot processes surrounding capillaries, astrocyte processes comprising the glial limiting membrane, in ependymal cells, and in subependymal astrocytes. Therefore, increased AQP4 in the splenial astrocyte may be an important role to early develop cytotoxic edema after SE.