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J Physiol Volume 556, Number 3, 905-917, May 1, 2004 DOI: 10.1113/jphysiol.2003.060079
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Subtypes of vagal afferent C-fibres in guinea-pig lungs

B. J. Undem1, B. Chuaychoo1, M.-G. Lee1, D. Weinreich2, A. C. Myers1 and M. Kollarik1

1 Johns Hopkins School of Medicine, and University, Baltimore, MD, USA2 University of Maryland School of Medicine, Baltimore, MD, USA

An ex vivo, vagally innervated, lung preparation was used to address the hypothesis that vagal C-fibres comprise at least two distinct phenotypes. Histological and extracellular electrophysiological experiments revealed that vagal C-fibres innervating the pulmonary system are derived from cell bodies situated in two distinct vagal sensory ganglia. The jugular (superior) ganglion neurones project C-fibres to both the extrapulmonary airways (larynx, trachea and bronchus) and the lung parenchymal tissue. By contrast, C-fibres from nodose (inferior) neurones innervate primarily structures within the lungs. Histologically, nodose neurones projecting lung C-fibres were different from the jugular neurones in that they were significantly less likely to express neurokinins. The nerve terminals within the lungs of both nodose and jugular C-fibres responded with action potential discharge to capsaicin and bradykinin application, but only the nodose C-fibre population responded with action potential discharge to the P2X selective receptor agonist {alpha},ß-methylene-ATP. Whole cell patch clamp recording of capsaicin-sensitive nodose and jugular ganglion neurones retrogradely labelled from the lung tissue revealed that, like the nerve terminals, lung specific nodose C-fibre neurones express functional P2X receptors, whereas lung specific jugular C-fibres do not. The data support the hypothesis that both neural crest-derived neurones (jugular ganglia) and placode-derived neurones (nodose ganglia) project C-fibres in the vagus, and that these two C-fibre populations represent distinct phenotypes.

(Received 18 December 2003; accepted after revision 16 February 2004; first published online 20 February 2004)
Corresponding Author J. Bradley: Johns Hopkins Asthma Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA. Email bundem{at}jhmi.edu




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