Fig. 3. Purinergic receptor agonists and antagonists confirm that the P2X7 receptor activates the ERKs.a, Purinergic agonists demonstrated a profile consistent with P2X7 receptor-induced ERK activation. ATP-γ-S, Adenosine 5′-O-[3-thiotriphosphate];2-MS-ATP, 2-methyl-thio-ATP; α-β-M-ATP, α-β-methylene ATP. The control level is the level of MAP kinase activation in untreated cultures and was defined as 0%. The level of ERK activation documented with the selective P2X7 receptor agonist Bz-ATP was defined as 100%. All compounds were applied for 15 min at a concentration of 100 μm. b, Purinergic receptor antagonists and the ERK antagonist PD98059 diminished ERK activation in response to P2X7 receptor stimulation. All cultures were subjected to 15 min of 100 μm Bz-ATP stimulation in the presence or absence of various signaling inhibitors. Concentrations and preincubation (PI) times of inhibitors were as follows: PD98059, 50 μm, 15 min PI; o-ATP, 300 μm, 2 hr PI; DIDS, 200 μm, 2 hr PI; PPADS, 100 μm, 15 min PI; Suramin, 1 mm, 15 min PI. o-ATP, Oxidized ATP; PPADS, pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid;DIDS, 4′,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. Asterisks indicate a significant decrease from the Bz-ATP sample group.