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Brain levels of adenosine are elevated during hypoxia. Through effects on adenosine receptors (A₁, A_2A, A_2B and A₃) on astrocytes, adenosine can influence functions such as glutamate uptake, reactive gliosis, swelling, as well as release of neurotrophic and neurotoxic factors having an impact on the outcome of metabolic stress. We have studied the roles of these receptors in astrocytes by evaluating their susceptibility to damage induced by oxygen deprivation or exposure to the hypoxia mimic cobalt chloride (CoCl₂). Hypoxia caused ATP breakdown and purine release, whereas CoCl₂ (0.8 mM) mainly reduced ATP by causing cell death in human D384 astrocytoma cells. Further experiments were conducted in primary astrocytes prepared from specific adenosine receptor knock-out (KO) and wild type (WT) mice. In WT cells purine release following CoCl₂ exposure was mainly due to nucleotide release …