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Figure 1 | Molecular Pain

Figure 1

From: Prostaglandin E2 potentiation of P2X3 receptor mediated currents in dorsal root ganglion neurons

Figure 1

Enhancement of fast-inactivating ATP currents by PGE2.

(A) PGE enhances P2X3 receptor-mediated ATP currents. α,β-meATP and ATP evoked similar fast-inactivating currents. Both currents were blocked by the specific P2X3 antagonist, A-317491.

(B) In the same cell, PGE2 potentiated α,β-meATP- and ATP-evoked currents similarly. Iαβ-meATP (PGE2)/Iαβ-meATP = 1.47 ± 0.07, IATP (PGE2)/IATP = 1.54 ± 0.06 (* P < 0.05, n = 8).

(C) Homomeric P2X3 receptors mediate the action of PGE2. (Left) A 2 sec ATP (10 μM) pulse elicited fast-inactivating (Fast), slow-inactivating (Slow) and mixed ATP currents in normal cells. Membrane was held at -60 mV. The currents were obtained from three different cells. (Right) After a 2-min application of PGE2 (1 μM), the fast ATP current was potentiated but the slow ATP current did not change. For the cell exhibiting mixed responses, PGE2 enhanced the peak, but not the steady state ATP currents. Bar graphs show the pooled data. PGE2 increased the peak amplitude of both fast-inactivating ATP currents [IATP (PGE2)/IATP = 1.46 ± 0.04 (n = 72)] and mixed ATP currents [IATP (PGE2)/IATP = 1.56 ± 0.08 (n = 6)] (* P < 0.05), which were mediated by homomeric P2X3 receptors. On the other hand, PGE2 had no effect on P2X2/3 receptor-mediated slow currents.

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