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. 2014 Jan 13;6(1):e00132. doi: 10.1042/AN20130040

Figure 2. Glutamate-stimulated ATP release from astrocytes requires GluK2 activation and ERK1/2 phosphorylation.

Figure 2

The cells were treated as described in Figure 1 with the addition of glutamate to a final concentration of 100 μM glutamate, and the inhibitor of ecto-ATPase, ARL67156, present in all experiments. Some experiments were performed in the additional presence of either 25 μM MPEP, an antagonist of mGluR5 and GluK2 receptors, or 10 μM U0126, a specific inhibitor of ERK phosphorylation (by inhibition of MEK). For undetermined reasons the ATP release in response to glutamate was smaller than in Figure 1, but the main result is that it was completely prevented by either inhibitor. Literature data indicate that mGluR5 is not functioning in differentiated cells. Results are averages of RLU values from three individual cultures. S.E.M. values are indicated by vertical bars. *Statistically significant (P<0.05) difference from all other groups.