ABSTRACT
Vagal C-fibers form a large majority of the afferent nerves innervating the
lungs and airways. These nerves show similar properties to those of the cutaneous C-fibers of somatic sensory populations (dorsal root ganglia
neurons) studied in relation to functional and anatomical aspects of nocice-
ptive transmission (1-3). The axons of C-fibers conducting nociceptive signals
are unmyelinated and their cell bodies are small in size. Their peripheral
terminals are specialized to detect painful (nociceptive) stimuli such as
heat, mechanical insults, and inflammatory mediators, and are also referred
to as nociceptors (4). Vagal C-fibers initiate bronchoconstriction and some
types of cough reflex (5,6), and are closely involved in key aspects of airway diseases associated with hypersensitivity (2,7). The application of nocicep-
tive stimuli to the airways results in excitation of airway C-fiber afferents
leading to the subsequent release of tachykinins and neuropeptides from
the fibers, thus causing local effects including smooth muscle contraction
(8). Application of capsaicin, a potent activator of a major population of
C-fibers, results in cough and neurogenic inflammation (1,9), and induces
a functional desensitization of these afferents and depletion of neuropeptides and substance P (SP) in the periphery during disease states (10-12).
Finally, large chronic doses of capsaicin reduce airway hypersensitivity to
diverse external stimuli (13,14).
