A characteristic feature of brain injury is the rapid reaction of microglia and astrocytes (1–3) (Fig. 1). Reactive astrocytes display hypertrophy, elevated glutamine synthetase, oxido-reductive enzyme activity, and accumulation of the astrocyte-specific structural protein, glial fibrillary acidic protein (GFAP) (2,4). Activated microglia are characterized by hypertrophy, proliferation, increased surface expression of immune marker molecules, increased migration, release of oxygen radicals and proteases, and differentiation into a macrophagelike phenotype (5–7). Such responses may be beneficial in the healing phases of central nervous system (CNS) injury by actively monitoring and controlling the extracellular environment, walling off areas of the CNS from non-CNS tissue, and removing dead or damage cells (3,5,8). This gliotic process, however, is also thought to impart detrimental consequences by collateral neuronal damage from released microglial cytotoxins and inhibit neuronal regeneration by physical or biochemical impediments (6,8–14). In various models of nervous system injury, brain ischemia, deafferentation, physical trauma, and excitotoxicity, glial cells become activated upon injury and emit an inflammatory-like response, including the release of pro-inflammatory cytokines.