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1 Department of Medicine, The Johns Hopkins Asthma and Allergy Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224; and 2 Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California Davis, Davis, California 95616
In the vagal-sensory system, neuropeptides
such as substance P and calcitonin gene-related peptide (CGRP) are
synthesized nearly exclusively in small-diameter nociceptive type
C-fiber neurons. By definition, these neurons are designed to respond to noxious or tissue-damaging stimuli. A common feature of visceral inflammation is the elevation in production of sensory neuropeptides. Little is known, however, about the physiological characteristics of
vagal sensory neurons induced by inflammation to produce substance P. In the present study, we show that allergic inflammation of guinea pig
airways leads to the induction of substance P and CGRP production in
large-diameter vagal sensory neurons. Electrophysiological and
anatomical evidence reveals that the peripheral terminals of these
neurons are low-threshold A
mechanosensors that are insensitive to nociceptive stimuli such as capsaicin and bradykinin. Thus inflammation causes a qualitative change in chemical coding of
vagal primary afferent neurons. The results support the hypothesis that
during an inflammatory reaction, sensory neuropeptide release from
primary afferent nerve endings in the periphery and central nervous
system does not require noxious or nociceptive stimuli but may also
occur simply as a result of stimulation of low-threshold mechanosensors. This may contribute to the heightened reflex physiology and pain that often accompany inflammatory diseases.
vagal neurons; nodose ganglion; jugular ganglion; capsaicin; mechanosensors; substance P
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