In the WAG/Rij rat, a model for human absence epilepsy, spike-wave discharges (SWD) and absence epileptic behavior develop after the age of 3 months. The rostral part of the reticular thalamic nucleus (rRTN) is involved in SWD. Ca2+ channels play a central role in the initiation and maintenance of burst firing activity of thalamic cells. We hypothesize that a changed expression of α1-subunits of one or more high voltage-activated Ca2+ channel types in the rRTN underlies the development of SWD. To test this hypothesis we compared 3- and 6-month-old WAG/Rij rats with nonepileptic, age-matched control rats. By immunocytochemistry, the expressions of α11.3-, α 12.1-, α12.2-, and α12.3-subunits were shown in both strains, demonstrating the presence of Cav1.3, Cav2.1, Cav2.2, and Cav2.3 channels, respectively. Quantification of channel expression indicates that the development of SWD in WAG/Rij rats is concomitant with an increased expression of Cav2.1 channels in the rRTN. These channels are mainly presynaptic, as revealed by double immunofluorescence involving the presynapse marker syntaxin. The mechanism by which this increase could be related to the occurrence of SWD has been discussed.
- ACI rat
- Ca 1.3-channels
- Double immunofluorescence
- Quantitative immunocytochemistry
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience