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Publication : Normal delay eyeblink conditioning in mice devoid of astrocytic S100B.

First Author  Kim HS Year  2011
Journal  Neurosci Lett Volume  489
Issue  3 Pages  148-53
PubMed ID  21146588 Mgi Jnum  J:278306
Mgi Id  MGI:6323280 Doi  10.1016/j.neulet.2010.12.005
Citation  Kim HS, et al. (2011) Normal delay eyeblink conditioning in mice devoid of astrocytic S100B. Neurosci Lett 489(3):148-53
abstractText  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.
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