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Department of Physiology, University of Kentucky Medical Center, Lexington, Kentucky 40536
Mediators of inflammation, such as PGE2, are known to sensitize the airways to inhaled irritants and circulating autacoids. Evidence from in vivo studies has shown the involvement of vagal pulmonary C-fiber afferents in the PGE2-elicited airway hypersensitivity. However, whether PGE2 acts directly on these sensory nerves is unclear. The present study aimed to investigate whether PGE2 has direct potentiating effects on nodose and jugular pulmonary C neurons cultured from adult Sprague-Dawley rats and, if so, determine whether the EP2 prostanoid receptor is involved. Pulmonary neurons were identified by retrograde labeling with a fluorescent tracer 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate. Using perforated patch-clamp technique, our results showed that 1) PGE2 pretreatment (1 µM) increased the whole cell current density elicited by capsaicin and phenylbiguanide, chemical agents known to stimulate pulmonary C fibers; 2) selective activation of the EP2 prostanoid receptor by butaprost (3-10 µM) increased the whole cell current density elicited by capsaicin; and 3) PGE2, as well as butaprost, increased the number of action potentials evoked by current injection. Therefore, we conclude that PGE2 directly sensitizes vagal pulmonary C neurons to chemical and electrical stimulation. Furthermore, butaprost modulates the neurons in a manner similar to that of PGE2, suggesting that the effects of PGE2 are mediated, at least in part, through the EP2 prostanoid receptor.
EP2 prostanoid receptor; butaprost; 1,1'-dioctadecyl-3,3, 3',3'-tetramethylindocarbocyanine perchlorate; nodose ganglion; jugular ganglion
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