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This Article Full Text Full Text (PDF) All Versions of this Article: 294/3/L563    most recent 00336.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ni, D. Articles by Lee, L.-Y. PubMed PubMed Citation Articles by Ni, D. Articles by Lee, L.-Y.

Effect of increasing temperature on TRPV1-mediated responses in isolated rat pulmonary sensory neurons

Department of Physiology, University of Kentucky Medical Center, Lexington, Kentucky

Submitted 20 August 2007 ; accepted in final form 1 January 2008

Hyperthermia has been shown to sensitize vagal pulmonary C-fibers in anesthetized rats. However, it was not clear whether the effect was due to a direct action of hyperthermia on these sensory neurons. To answer this question, we carried out this study to determine the effect of increasing temperature on the responses to various chemical stimuli in isolated nodose and jugular ganglion neurons innervating the rat lungs. In the whole cell perforated patch-clamp study, when the temperature was increased from normal (36°C) to hyperthermic (40.6°C) level of the rat body temperature, the inward currents evoked by capsaicin, a selective activator of the transient receptor potential vanilloid type 1 (TRPV1), and 2-aminoethoxydiphenyl borate (2-APB), a nonselective activator of TRPV1–3 receptors, were both significantly increased. This potentiating effect was clearly present even at a moderate level of hyperthermia (39°C). However, only the slow, sustained component of acid-evoked current mediated through the TRPV1 receptor was potentiated by hyperthermia, whereas the rapid, transient component was inhibited. In contrast, the currents evoked by adenosine 5'-triphosphate and acetylcholine, neither of which is known to activate the TRPV1 channel, did not increase when the same temperature elevation was applied. Furthermore, the hyperthermia-induced potentiation of the cell response to 2-APB was significantly attenuated by either capsazepine or AMG 9810, selective TRPV1 antagonists. In conclusion, increasing temperature within the physiological range exerts a potentiating effect on the response to TRPV1 activators in these neurons, which is probably mediated through a positive interaction between hyperthermia and these chemical activators at the TRPV1 channel.

C-fibers; transient receptor potential vanilloid channel; acid-sensing ion channel; exercise; inflammation