Research reportCorrelation between content of high-energy phosphates and hypoxic-ischemic damage in immature and mature astrocytes
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Cited by (52)
A sensitive HPLC-based method to quantify adenine nucleotides in primary astrocyte cell cultures
2012, Journal of Chromatography B: Analytical Technologies in the Biomedical and Life SciencesCitation Excerpt :We found that ATP, ADP, AMP levels, and the AEC in control astrocyte cultures were 25.4 ± 2.93, 4.59 ± 0.77, 0.22 ± 0.07, and 0.92 ± 0.02, respectively. These values are in agreement with other published values found in astrocyte cultures or astocytoma cell lines using alternative methods or pooling of samples [20–27]. In this study, the cells were flash frozen in liquid nitrogen and extracted on dry ice to prevent the loss of ATP due to enzymatic conversion to ADP and AMP.
Effects of continuous hypoxia on energy metabolism in cultured cerebro-cortical neurons
2008, Brain ResearchCitation Excerpt :It is possible that surviving neurons possess a more immature and thus more anoxia-tolerant phenotype. Astrocytes in primary culture respond to hypoxic conditions by up-regulation of glycolysis (Callahan et al., 1990; Tholey et al., 1991;Sochocka et al., 1994; Yager et al., 1994; Swanson and Benington, 1996; Niitsu et al., 1999; Marrif and Juurlink, 1999). This might aid in maintaining the intracellular ATP levels in hypoxic astrocytic cultures at levels sufficient for survival (Yager et al., 1994).
Bioenergetics of cerebral ischemia: A cellular perspective
2008, NeuropharmacologyCitation Excerpt :Cultured cortical astrocytes survive oxygen–glucose deprivation for a very long time in balanced media, reflecting (i) their capacity to survive on either glycolytically or oxidatively derived energy; (ii) their ability to greatly increase glycolysis during anoxia in mature cells (Walz and Mukerji, 1990), but in contrast to neurons not in immature cells (Fig. 4) (Peng and Hertz, unpublished experiments); (iii) their ability to efficiently oxidize other substrates than glucose (Yu and Hertz, 1983; Edmond et al., 1987; Edmond, 1992; Hertz, 2003; Hertz and Hertz, 2003); (iv) their upregulation of a number of glycolytic enzymes (Tholey et al., 1991; Marrif and Juurlink, 1999; Niitsu et al., 1999) after a few hours of hypoxia; and (v) their high glutathione content that make them relatively resistant to reactive oxygen species (Juurlink, 1997), although the resistance is not complete (Hori et al., 1994), and it is reduced by glutathione depletion (Sims et al., 2004; Gabryel and Małecki, 2006). During incubation under physiological conditions they only die during simulated ischemia once their ATP supplies have been exhausted (Gregory et al., 1990; Yager et al., 1994; Hertz et al., 1995; Swanson and Benington, 1996; Cotrina et al., 1998; Voloboueva et al., 2007), and cell death is delayed by hyperglycemia (Table 1) (Kelleher et al., 1993). They also maintain glutamate uptake for a long time (Swanson, 1992; Huang et al., 1993), and in neuronal–astrocytic co-cultures specific inhibition of oxidative metabolism in astrocytes increases neuronal vulnerability to glutamate toxicity, probably by inhibiting uptake of released glutamate (Voloboueva et al., 2007).
Intracerebroventricular administration of creatine protects against damage by global cerebral ischemia in rat
2006, Brain ResearchCitation Excerpt :One of the most important determinants of irreversible brain ischemic damage is decreased ATP (Lipton and Whittingham, 1982; Obrenovitch et al., 1988; Yager et al., 1994).
Seasonal differences and protection by creatine or arginine pretreatment in ischemia of mammalian and molluscan neurons in vitro
2004, Brain ResearchCitation Excerpt :During anoxia or ischemia, ATP decrease is slowed by the creatine/phosphocreatine system. Cell death does not occur as long as the ATP content remains above 25% of control [26]. This may have important clinical implications because the maintenance of a sufficient ATP content by the phosphocreatine pool could have protective action.