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. 2009 Jan;108(2):331–340. doi: 10.1111/j.1471-4159.2008.05761.x

Fig. 1.

Fig. 1

Potentiation of P2X1 receptor currents by PMA and mGluR1α receptor stimulation is sensitive to inhibitors of novel isoforms of protein kinase C. (a) Representative traces of currents evoked by ATP (100 μM) under control conditions (left) and following treatment with PMA (100 nM) or PMA following incubation with the PKC inhibitors (1 h pre-incubation before 10 min of PMA) calphostin C (1 μM), K252a (100 nM), Gö6983 (200 nM) or Gö6976 (200 nM). The lower panel shows a summary of the effects of the inhibitors on PMA potentiation, n=5–19. (b) Sample traces of the effects of PKC inhibitors and mGluR1α mediated potentiation of P2X1 receptor currents. Application of glutamate (100 μM) evoked a transient inward calcium activated chloride current and potentiated the subsequent ATP current. Potentiation was reduced following pre-treatment of the oocytes with the PKC inhibitors. The lower panel shows a summary of the effects, of the inhibitors on glutamate potentiation, n=3–13. ***p< 0.001.