Mytochondrial dysfunction in astrocytes: A target for neuronal protection from glucose deprivation.

Glucose is considered to be the major nutrient for cells of the adult nervous system. Although the weight of the mature brain is only 2-3% of the total body weight, this organ may consume up to one fourth of the body¿s glucose supply (Clarke and Sokoloff, 1994). Only a small portion of this glucose is used for biosyntheses (inositol and glycoconjugates) and by far the major part is consumed in energy metabolism. Nervous tissue is most sensitive towards deviations in normal blood glucose levels, and a lack in glucose supply results almost instantaneously in severe disturbances of brain functions (Sieber and Traystman, 1992), in unconsciousness and ultimately in death. It seems like that glucose is extremely important for maintaining normal cell functions. For instance, the presence of glucose in astroglial cells cocultured with neurons improved neuronal survival (Swanson and Choi, 1993), and withdrawal of glucose induces cell swelling, increased oxidative stress, cytokines and chemokines release in astrocytes (Papadopoulos et al., 1997; Ouyang et al., 2006). Free radical injury of astrocytes may impair their ability to regulate extracellular glutamate or K+, reduce their ability to defend against oxidative stress and therefore increase the likelihood of neuronal loss.