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Evaluation of Voltage‐Activated Calcium Channel α‐1G Subunit Expression in Genetic Absence Epilepsy Rats
Author(s) -
AKIN DEMET,
KETENCI SEMA,
SIRVANCI SERAP,
ONAT FILIZ
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb409
Subject(s) - calcium channel , protein subunit , hippocampus , voltage dependent calcium channel , globus pallidus , striatum , epilepsy , neuroscience , medicine , chemistry , endocrinology , thalamus , l type calcium channel , biology , calcium , basal ganglia , central nervous system , biochemistry , dopamine , gene
T‐type voltage‐activated calcium channels play an essential role in the generation of absence seizures. It is well known that thalamocortical circuit is critically involved in the propagation of spontaneous spike and wave discharges (SWDs) in Genetic absence epilepsy rats from Strasbourg (GAERS). Calcium channel α‐1G subunit expression was studied by immunohistochemical methods in the hippocampus (CA1, CA3, dentate gyrus), lateral and medial thalamic regions, globus pallidus and striatum of control Wistar rats (n=5) and GAERS (n=4). The brains were removed after perfusion and brain slices (40 mm) were incubated with antibodies against calcium channel α‐1G subunit. Peroxidase activity was visualized by 0.03 % 3‐3‐diaminobenzidine. We used semi‐quantitative scoring and analyzed the data with unpaired t test. We found decreased α‐1G subunit immunolabeling in the lateral thalamic region of GAERS animals compared with control Wistar rats. No difference was observed in any of the other areas between Wistar rats and GAERS. These results show that decreased calcium channel α‐1G subunit expression in lateral thalamic regions may play a role in the mechanisms underlying absence seizures. Further experiments will be performed to investigate the expression of other calcium channel subunits. Supports: Istanbul Bilim University and Marmara University S.R.C.SAG‐A 090409‐0072