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Normal delay eyeblink conditioning in mice devoid of astrocytic S100B
Hye-Soo R Kim1, Akiko Seto-Ohshima, Hiroshi Nishiyama
1Laboratory for Behavioral Genetics, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako 351-0198, Japan.
Neuroscience Letters
|December 15, 2010
Summary
Mice lacking S100B protein show improved learning and memory in the hippocampus but not in the cerebellum. This suggests S100B protein plays a different role in distinct brain regions.
Area of Science:
- Neuroscience
- Molecular Biology
- Astrocytes Biology
Background:
- S100B is a calcium-binding protein primarily secreted by astrocytes.
- Mice lacking S100B (S100B-KO) show enhanced hippocampal long-term potentiation and memory.
- Bergmann glia in the cerebellum express high levels of S100B.
Purpose of the Study:
- To investigate the role of S100B in cerebellar function.
- To compare S100B's function in the hippocampus versus the cerebellum.
Main Methods:
- Utilized S100B-knockout (S100B-KO) mice.
- Assessed hippocampus-dependent learning and memory tasks.
- Evaluated cerebellum-dependent motor coordination and learning using delay eyeblink conditioning.
Main Results:
- S100B-KO mice showed no anatomical brain abnormalities.
- S100B-KO mice performed similarly to wild-type mice in cerebellum-dependent tasks.
- S100B's crucial role in hippocampal plasticity was confirmed, but not in the cerebellum.
Conclusions:
- S100B protein has differential roles in hippocampal and cerebellar function.
- S100B is essential for hippocampal neuronal plasticity but not for cerebellar motor coordination or learning.
