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This Article Full Text Full Text (PDF) All Versions of this Article: 575/2/481    most recent jphysiol.2006.109371v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chuaychoo, B. Articles by Undem, B. J. Search for Related Content PubMed PubMed Citation Articles by Chuaychoo, B. Articles by Undem, B. J. Related Collections Neuroscience

¹ Johns Hopkins School of Medicine
² National Institutes of Aging, Baltimore, MD, USA

We addressed the hypothesis that single vagal afferent C-fibres can be stimulated via either the adenosine A₁ or A_2A receptor subtypes. The effect of adenosine on the nerve terminals of vagal sensory nerve subtypes was evaluated in an ex vivo perfused guinea pig lung preparation using extracellular recording techniques. Adenosine (10 µM) consistently evoked action potential discharge in lung C-fibre terminals arising from the nodose ganglia, but failed to evoke action potential discharge in most jugular ganglion C-fibres. Adenosine also failed to activate stretch-sensitive nodose A-fibres in the lungs. The selective A₁ antagonist DPCPX (0.1 µM) or the selective A_2A antagonist SCH 58261 (0.1 µM) partially inhibited the nodose C-fibre activation by adenosine, and the combination of both antagonists almost completely inhibited the response. The adenosine-induced action potential discharge in nodose C-fibres was mimicked by either the selective A₁ agonist CCPA (1 µM) or the selective A_2A agonist CGS 21680 (1 µM). Single cell PCR techniques revealed that adenosine A₁ and A_2A receptor mRNA was expressed in individual nodose neurons retrogradely labelled from the lungs. The gramicidin-perforated patch clamp technique on neurons retrogradely labelled from the lungs was employed to study the functional consequence of adenosine receptor agonists directly on neuronal membrane properties. Both the selective A₁ agonist CCPA (1 µM) and the selective A_2A agonist CGS 21680 (1 µM) depolarized the airway-specific, capsaicin-sensitive, nodose neurons to action potential threshold. The data support the hypothesis that adenosine selectively depolarizes vagal nodose C-fibre terminals in the lungs to action potential threshold, by stimulation of both adenosine A₁ and A_2A receptor subtypes located in the neuronal membrane.

(Received 9 March 2006; accepted after revision 6 June 2006; first published online 15 June 2006)
Corresponding author B. J. Undem: Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA. Email: bundem{at}jhmi.edu

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