Abstract
S100B is a small calcium- and zinc-binding protein expressed by astrocytes in the central nervous system. Here, we examined the role of S100B in epileptogenesis using an amygdala kindling paradigm comparing S100B knockout mice with their wild-type counterparts. Astrocyte activation following kindling, assessed by glial fibrillary acidic protein expression in the hippocampus and amygdala, was similar in wild-type and knockout mice. In addition, wild-type and knockout mice did not have substantially different afterdischarge thresholds. However, knockout mice kindled more rapidly and exhibited more severe seizures. These results implicate normal levels of S100B in the attenuation of epileptogenesis.
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