Figure 3
SOD1G93A astrocytes exhibit ATP-dependent neurotoxicity, proliferation, and increased ATP degradation. (A) Motor neuron survival in co-culture with SOD1G93A astrocytes pre-treated for 48 hours with the P2X7r inhibitor BBG (1 μM) or the ATP-hydrolyzing enzyme apyrase (5 U/ml) (B) Effect of apyrase treatment on SOD1G93A astrocyte proliferation in culture. (C) Degradation of exogenously added ATP by SOD1G93A or non-transgenic astrocytes astrocytes. Data are expressed as percentage of non-transgenic control, mean ± SEM from at least three independent experiments. Data are expressed as percentage of non-transgenic control, mean ± SEM from at least three independent experiments. *p < 0.05, significantly different from non-transgenic control.