Figure 3

Potentiation of GABA _A R-mediated currents by ATP and analogs does not require activation of ecto-protein kinase or P2 receptors in cultured hippocampal neurons. Representative individual whole-cell GABA current traces were taken 5 min before (Control) and after drug applications (100 μM, pulse-pressure ejection). A and B, AMP-PNP (2 mM; A) or ADP (2 mM; B), two ATP analogues that cannot function as phosphate donor for ecto-protein kinase mediated phosphorylation, remain capable of potentiating GABA currents, increasing the peak currents by 134.2 ± 11.4% (A; P < 0.05; n = 5) and 140 ± 14.7 (B; P < 0.05; n = 7), respectively. C, Non selective P2 receptor antagonist suramin (100 μM) and selective P2X₇ receptor antagonist BBG (1 μM) suppressed basal GABA currents on their own, but failed to prevent ATP from potentiating the currents; ATP increased the peak currents by 138.5 ± 16.5% (n = 5; P < 0.05) in the presence of both antagonists.