Potential involvement of S100B in the protective effects of a serotonin-1a agonist on ethanol-treated astrocytes

Previously, this laboratory found that the offspring of rats that consumed ethanol on a chronic basis prior to parturition exhibited a significant reduction in serotonin (5-HT) neurons and in astrocytes proximal to these neurons. This laboratory also showed that maternal treatment with a 5-HT1A agonist during the latter part of gestation prevented the reduction of 5-HT neurons and most of the astrocyte abnormalities. The present in vitro studies extended our prior in vivo work by examining the potential involvement of S100B with the protective effects of a 5-HT1A agonist, i.e., buspirone, on astrocytes. Astrocyte cultures were either maintained in chemically defined media in the presence and absence of ethanol and buspirone or in conditioned media that was generated by ethanol- and buspirone-treated astrocytes. A mouse monoclonal antibody to S100B was used to assess the potential involvement of S100B with the protective effects of buspirone. Additional in vitro studies measured the direct effects of S100B and ethanol on astrocyte proliferation. These investigations demonstrate that in vitro ethanol exposure reduces the number of astrocytes, and that treatment with the 5-HT1A agonist buspirone prevents the ethanol-associated reduction in astrocyte number. The protective effects of buspirone appear to be mediated by factors that are secreted by astrocytes; such factors likely include S100B. In addition, added S100B prevents an ethanol-associated reduction in [H-3]-thymidine incorporation into proliferating astrocytes. (C) 2001 Elsevier Science B.V. All rights reserved.