Changes in astrocyte markers, such as glial fibrillary acidic protein (GFAP), are found in brains of mouse models and in postmortem brains of humans with different neuropsychiatric diseases or in response to various drugs of abuse (Kim et al., 2017). Changes in GFAP are associated with impaired astrocyte function involving glutamate uptake, neuronal-glial signaling, and release of inflammatory mediators or neurotrophic factors that signal the surrounding parenchyma to resolve or prolong inflammation (Pekny and Pekna, 2014). Inflammatory insults may consequently induce discrete or widespread alterations in astrocyte gene expression, creating a graded continuum through which astrocytes respond to various pathological conditions in the CNS (Zamanian et al., 2012). Like microglia, astrocytes are less homogeneous than previously thought, with subtypes of activated astrocytes showing differential effects (Liddelow et al., 2017). Evidence of brain-region heterogeneity among different populations (Chai et al., 2017; Martín-Fernández et al., 2017; Srinivasan et al., 2016) suggests that this is important for astrocyte reactivity and functional effects. Not all astrocytes express GFAP (Oberheim et al., 2012), and thus new molecular markers associated with the different phenotypes and activated states are needed.
