期刊
JOURNAL OF NEUROSCIENCE
卷 28, 期 43, 页码 10928-10936出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3693-08.2008
关键词
glia; hippocampus; mGluR3; local field potential; seizure; neuron-glia interactions
资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [18053026]
- Human Frontier Science Program [RGY0073/2006]
- RIKEN Brain Science Institute
- Grants-in-Aid for Scientific Research [18053026] Funding Source: KAKEN
S100B is the principal calcium-binding protein of astrocytes and known to be secreted to extracellular space. Although secreted S100B has been reported to promote neurite extension and cell survival via its receptor [receptor for advanced glycation end products (RAGE)], effects of extracellular S100B on neural activity have been mostly unexplored. Here, we demonstrate that secreted S100B enhances kainate-induced gamma oscillations. Local infusion of S100B in S100B(-/-) mice enhanced hippocampal kainate-induced gamma oscillations in vivo. In a complementary set of experiments, local application of anti-S100B antibody in wild-type mice attenuated the gamma oscillations. Both results indicate that the presence of extracellular S100B enhances the kainate-induced gamma oscillations. In acutely isolated hippocampal slices, kainate application increased S100B secretion in a neural-activity-dependent manner. Further pharmacological experiments revealed that S100B secretion was critically dependent on presynaptic release of neurotransmitter and activation of metabotropic glutamate receptor 3. Moreover, the kainate-induced gamma oscillations were attenuated by the genetic deletion or antibody blockade of RAGE in vivo. These results suggest RAGE activation by S100B enhances the gamma oscillations. Together, we propose a novel pathway of neuron-glia communications - astrocytic release of S100B modulates neural network activity through RAGE activation.
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