Objectives: The role of white matter astrocytes in absence epilepsy is unknown. The present study aims to quantify astrocytic markers glial fibrillary acidic protein (GFAP), gap junction's proteins connexin 30 (Cx30) and connexin 43 (Cx43) in the corpus callosum (CC) of genetic absence epileptic rats from Strasbourg (GAERS), Wistar albino glaxo rats from Rijswijk (WAG/Rij)and compare the results with control animals.
Methods: -The density of GFAP, Cx30 and Cx43 positive astrocytes in per unite area were quantified in the CC of GAERS, WAG/Rij and control animals using immunohistochemistry and real-time quantitative polymerase chain reaction (RT-qPCR). The quantifications were made from three regions of CC; below the primary somatosensory (S1BF), below the motor (M1) and below the retrosplenial (RSG) cortices.
Results: oThe number GFAP, Cx30 and Cx43 immunopositive astrocytes showed heterogeneous distribution within the CC. The GFAP immunopositive astrocytes was significantly high in the S1BF region of the three strains. The immunopositive GFAP and Cx43 showed significant decrease in the S1BF and M1 regions in GAERS and WAG/Rij compared to control animals, however, an increase in the immunopositive Cx30 was observed in the same regions in both GAERS and WAG/Rij compared to control Wistar animals but the increase was significant for GAERS but not for WAG/Rij. The RT-qPCR analysis was corroborated by GFAP immunohistochemistry results.
Conclusion: The different expression pattern of the two Cx's in the CC of the epileptic strains compared to control animals may indicate a compensatory response or maybe the cause of generalization of absence seizures.
Keywords: Corpus callosum; absence epilepsy; connexin; glial fibrillary acidic protein; immunohistochemistry; rt-qPCR.