Abstract
S100B is predominantly synthesized by astrocytes and secreted to the extracellular space. The secreted S100B exerts various effects through the activation of receptor for advanced glycation end-products (RAGE). We have previously shown that the amplitude of kainate-induced gamma oscillation in hippocampal CA1 stratum radiatum is significantly smaller in S100B knockout (KO) mice.To assess the contribution of extracellular S100B to the gamma oscillation, we performed local field potential recording with local infusion of S100B at CA1 str. radiatum in S100B KO mice in vivo. While local infusion of 10 μM S100B resulted in an increase of the gamma oscillation, rescuing S100B knockout effect. Post-hoc immunohistochemical observation indicated that the infused S100B was not taken up by astrocytes. In a separate set of experiments, we locally applied anti-S100B antibody for functional blockade in wild-type (WT) mice, resulting in a decreased amplitude of the gamma oscillation. Both results indicate that the presence of extracellular S100B contributes to the increased gamma oscillation. Next, we asked whether the effect of extracellular S100B was due to activation of S100B receptors. The amplitude of kainate-induced gamma oscillation at CA1 str. radiatum decreased significantly by blocking RAGE in WT mice. Furthermore, co-application of S100B and anti-RAGE antibody in S100B KO mice abolished the effect of S100B on the gamma oscillation. These data suggest that activation of RAGE significantly contributes to the increased gamma oscillation. [J Physiol Sci. 2008;58 Suppl:S124]
