作者: M. Brozmanova , F. Ru , L. Surdenikova , L. Mazurova , T. Taylor-Clark
DOI: 10.1111/J.1365-2982.2011.01768.X
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摘要: Background The TRPA1 receptor is directly activated by a wide range of chemicals including many endogenous molecules relevant for esophageal pathophysiology. We addressed the hypothesis that agonists differentially activate nociceptive subtypes depending on their embryological source (neural crest or epibranchial placodes). Methods Single cell RT-PCR and whole patch clamp recordings were performed vagal neurons retrogradely labeled from guinea pig esophagus. Extracellular made in isolated innervated esophagus preparation ex vivo. Key Results revealed majority nodose (placodes-derived) jugular crest-derived) TRPV1-positive nociceptors express TRPA1. fiber recording showed allyl-isothiocyanate (AITC) cinnamaldehyde effective inducing robust action potential discharge nerve terminals nociceptors, but had far less effect (approximately fivefold less). Higher efficacy to was confirmed esophagus-labeled studies. Similarly neural crest-derived spinal DRG are also only modestly allyl-isothiocyanate. Conclusions & Inferences conclude substantially more activators placodes-derived than nociceptors. Our data predict diseases presence will be preferentially signaled