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Enhanced excitability of rat vagal pulmonary sensory neurons during hyperthermia
Author(s) -
Ni Dan,
Lee LuYuan
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a920-c
Subject(s) - hyperthermia , trpv1 , capsaicin , chemistry , sensory nerve , nodose ganglion , medicine , vagus nerve , respiratory system , anesthesia , transient receptor potential channel , sensory system , receptor , endocrinology , neuroscience , biology , stimulation
Tissue hyperthermia can occur in the lungs and airways under pathophysiological conditions and/or heavy exercises. However, the effect of hyperthermia on the activation of respiratory sensory afferent is not clear. A recent study in our lab showed that hyperthermia exerts both stimulatory and sensitizing effect on vagal pulmonary C‐fibers (J. Physiol. 565:, 2005). However, whether the sensitizing effect of hyperthermia is due to its direct action on these neurons is not known. To answer this question, we carried out this experiment to determine the effect of hyperthermia on the responses to various chemical stimuli of the nodose and jugular ganglion neurons innervating the lungs and airways of adult SD rats, and the possible involvement of TRPV channels. In the whole‐cell perforated patch clamp study, when the temperature was increased from 36 – 40 °C, the inward currents evoked by capsaicin (0.3 μM), proton (pH 5.5 or 6) and 2APB (0.3 mM) was increased by 190 ± 44% ( p < 0.01; n = 7), 123 ± 51% ( p < 0.01; n = 9) and 76 ± 11% ( p < 0.0001; n = 8), respectively; all three chemical agents activate transient receptor potential vanilloid receptor 1 (TRPV1). These results suggest that hyperthermia can exert a direct sensitizing effect on isolated vagal pulmonary sensory neurons, which may explain the hyperthermia‐induced hypersensitivity of vagal pulmonary nerve activity in anesthetized rats. Furthermore, this potentiating effect probably results from a positive interaction between hyperthermia and the activator of the TRPV1. Supported by NIH grant HL 67379