S100Bを介したニューロン—グリア相互作用
詳細
S100B is a brain specific calcium binding protein predominantly expressed in astrocytes. Previous studies using gene manipulated animals have suggested that the protein has a role in synaptic plasticity and learning. In order to assess the physiological roles of the protein in active neural circuitry, we have recorded spontaneous neural activities from the neocortex and hippocampus in urethane anesthetized S100B knockout (KO) and wildtype control (WT) mice. Typically occurring local field oscillation patterns including the slow (0.5-2 Hz) oscillations in the neocortex, theta (3-8 Hz) and sharp wave associated fast ripple (120-180 Hz) oscillations in the hippocampus were observed in both genotypes and appeared virtually indistinguishable. When seizure was induced by intraperitoneal injection of kainic acid, gamma (30-80 Hz) oscillation in hippocampal CA1 stratum radiatum was significantly smaller in S100B KO mice [1]. The results suggest that deficiency of S100B does not have a profound impact on spontaneous neural activity in normal conditions. However, when neural activity was sufficiently raised, activation of S100B related pathways may take effect, resulting in modulation of neural activities. As S100B is known to be secreted to the extracellular space by astrocytes, we have performed a series of S100B infusion and antibody blockade experiments. Our current results suggest that the attenuation of kainate induced gamma oscillation is likely to be an extracellular effect of S100B.[1] Sakatani et al., EJN 25:1144-1154 (2007) [J Physiol Sci. 2008;58 Suppl:S11]
