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Effect of olvanil and anandamide on vagal C‐fiber subtypes in guinea pig lung
Author(s) -
Lee MinGoo,
Weinreich Daniel,
Undem Bradley J
Publication year - 2005
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0706339
Subject(s) - trpv1 , capsaicin , chemistry , nodose ganglion , medicine , endocrinology , anesthesia , transient receptor potential channel , receptor , pharmacology , vagus nerve , stimulation
Certain fatty acid amides such as anandamide (AEA) and olvanil are agonists for the transient receptor potential, vanilloid‐1 (TRPV1) receptor, but have been found to activate TRPV1‐containing C‐fibers in some tissues but not others. We used extracellular recording and whole‐cell patch clamp techniques to investigate the effect of olvanil and AEA on different types of vagal C‐fibers innervating the same tissue, namely jugular and nodose vagal C‐fibers in guinea pig lungs. A 30 s exposure to AEA and olvanil caused action potential discharge in all nodose C‐fiber innervating lung but failed to activate jugular C‐fibers innervating lung and airways. The activation of nodose C‐fibers was blocked by the TRPV1 antagonist iodo‐resiniferatoxin. In whole‐cell patch clamp recordings of dissociated nodose and jugular capsaicin‐sensitive neurons labeled from lungs and airways, olvanil induced large TRPV1‐dependent inward currents in cell bodies of both nodose and jugular ganglion neurons. Prolonged exposure (up to 5 min) to olvanil caused action potential discharge in jugular C‐fiber innervating lung but the onset latency was four times longer in jugular than in nodose C‐fibers. The onsets of capsaicin response in nodose and jugular C‐fibers were not different. Decreasing the tissue temperature to 25°C increased the onset latency of olvanil‐induced activation of nodose C‐fibers 2–3‐fold, but did not effect the latency of the capsaicin response. Capsaicin, olvanil, and AEA stimulate jugular C‐fibers leading to tachykinergic contractions of isolated bronchi. The time to reach half‐maximum is more than four times longer for olvanil and AEA, as compared to capsaicin in evoking contractions. We conclude that brief exposure to certain fatty acid amides, such as AEA and olvanil activate nodose but not jugular C‐fiber terminals in the lungs. We hypothesize that this is because the nodose C‐fiber terminals are equipped with a temperature‐dependent mechanism for effectively and rapidly transporting the TRPV1 agonists so that they gain access to the intracellular binding sites on TRPV1. This transport mechanism may be differently expressed in two distinct subtypes of pulmonary C‐fiber terminals innervating the same tissue.British Journal of Pharmacology (2005) 146 , 596–603. doi: 10.1038/sj.bjp.0706339

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