Potentiation of GABA
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.