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. 2011 Jun 8;301(3):C587–C600. doi: 10.1152/ajpcell.00465.2010

Fig. 5.

Fig. 5.

Lack of modulation of TRPA1- but not TRPV1-mediated currents by activation of PKC and PKA pathways. A: increase in amplitude of AITC (20 μM)-induced currents with repeated applications. B: AITC (20 μM)-induced currents in the presence of the PKC activator phorbol 12,13-dibutyrate (PDBu; 1 μM). C: plot comparing the normalized amplitude of AITC-induced currents in the presence (■) or absence (▴) of PDBu. D: AITC (20 μM)-induced currents in the presence of PKA-activating cocktail [forskolin (FSK), 50 μM + IBMX, 50 μM]. E: plot comparing the normalized amplitude of AITC-induced currents in the presence (●) or absence (■) of FSK (50 μM) + IBMX (50 μM). F: capsaicin (30 nM)-induced current amplitude remained constant with repeated application. G: capsaicin (30 nM)-induced currents were significantly potentiated following the application of PDBu (1 μM) or FSK (50 μM) + IBMX (50 μM). H: plot comparing the normalized amplitude of capsaicin-induced currents in the absence (▴) or presence of PDBu (■) or FSK + IBMX (●).

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