Normal delay eyeblink conditioning in mice devoid of astrocytic S100B.

S100B is a small calcium binding protein synthesized and secreted mostly by astrocytes. Mice devoid of S100B (S100B-KO) develop without detectable anatomic abnormalities of the brain, but exhibit enhanced hippocampal long-term potentiation and enhanced performance in hippocampus-dependent learning and memory tasks, indicating that S100B has a crucial role in hippocampal neuronal plasticity. In the present study, we examined whether S100B has a similar role in the cerebellar regions, because Bergmann glia, a specialized subset of astrocytes in the cerebellar cortex, express a particularly large amount of S100B under physiologic conditions. Unlike in the hippocampus-dependent tasks, S100B-KO mice were indistinguishable from wild-type mice in both cerebellum-dependent motor coordination and delay eyeblink conditioning, a well-established paradigm for cerebellum-dependent learning and memory. These results suggest that S100B has differential roles in the hippocampus and cerebellum.