Alcohol sedation in adult is regulated by ?in cortex glia.

Although numerous studies have demonstrated that neuronal mechanisms regulate alcohol-related behaviors， very few have investigated the direct role of glia in behavioral responses to alcohol. The results described here begin to fill this gap in the alcohol behavior and gliobiology fields. Since exhibit conserved behavioral responses to alcohol and their CNS glia are similar to mammalian CNS glia， we used to begin exploring the role of glia in alcohol behavior. We found that knockdown of () in glia increased alcohol sedation and that this effect was specific to cortex glia and adulthood. These data implicate and?cortex glia in alcohol-related behaviors. Cortex glia are functionally homologous to mammalian astrocytes and Cp1 is orthologous to mammalian Cathepsin L. Our studies raise the possibility that cathepsins may influence behavioral responses to alcohol in mammals via roles in astrocytes.