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The Journal of Neuroscience, October 22, 2008, 28(43):10928-10936; doi:10.1523/JNEUROSCI.3693-08.2008

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Cellular/Molecular
Neural-Activity-Dependent Release of S100B from Astrocytes Enhances Kainate-Induced Gamma Oscillations In Vivo

Seiichi Sakatani,¹ Akiko Seto-Ohshima,² Yoshiaki Shinohara,¹ Yasuhiko Yamamoto,³ Hiroshi Yamamoto,³ Shigeyoshi Itohara,² and Hajime Hirase¹

¹Hirase Research Unit, Neuronal Circuit Mechanisms Research Group, and ²Laboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan, ³Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-0864, Japan

Correspondence should be addressed to either of the following at the same address: Seiichi Sakatani or Hajime Hirase, RIKEN Brain Science Institute, Neuronal Circuit Mechanisms Research Group, Wako-shi, 351-0198, Japan. Email: sakatani{at}brain.riken.jp or Email: hirase{at}brain.riken.jp

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.

Key words: glia; hippocampus; mGluR3; local field potential; seizure; neuron–glia interactions

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Received Aug. 4, 2008; accepted Sept. 13, 2008.

Correspondence should be addressed to either of the following at the same address: Seiichi Sakatani or Hajime Hirase, RIKEN Brain Science Institute, Neuronal Circuit Mechanisms Research Group, Wako-shi, 351-0198, Japan. Email: sakatani{at}brain.riken.jp or Email: hirase{at}brain.riken.jp

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