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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Pulm Pharmacol Ther. 2015 Jun 19;35:94–99. doi: 10.1016/j.pupt.2015.06.003

Fig. 2. Antimycin A increases nociceptive bronchopulmonary C-fibers excitability.

Fig. 2

A, representative traces of action potential discharge evoked by 10s challenge with α,β mATP (P2X2/3 agonist, 30 µM) in a nociceptive bronchopulmonary Cfiber before (control, A1) and 10 minutes after treatment with antimycin A (20 µM, A2). B, mean ± SEM response to 2nd application of α, β mATP (30 µM) normalized to response to 1st application of α, β mATP prior to either vehicle (white bar) or antimycin A (20 µM, black bars) in nociceptive C-fibers. The roles of ROS and PKC in hyperexcitability to α, β mATP were determined using pretreatment with DTT (1mM), NAC (1mM), GSH (1mM), myxothiazol (500 nM), BIM I (1 µM) or BIM V (1 µM). * Significant increase in 2nd α, β mATP-induced responses after antimycin A compared to vehicle (p<0.05). # Significant reduction in antimycin A-induced hyperexcitability to α, β mATP (p<0.05). Adapted from [49].