Interganglionic segregation of distinct vagal afferent fibre phenotypes in guinea-pig airways.
1. The present study addressed the hypothesis that jugular and nodose vagal ganglia contain the somata of functionally and anatomically distinct airway afferent fibres. 2. Anatomical investigations were performed by injecting guinea-pig airways with the neuronal tracer Fast Blue. The animals were killed 7 days later, and the ganglia were removed and immunostained with antisera against substance P (SP) and neurofilament protein (NF). In the nodose ganglion, NF-immunoreactive neurones accounted for about 98% of the Fast Blue-labelled cells while in the jugular ganglion they accounted for approximately 48%. SP and NF immunoreactivity was never (n = 100) observed in the same cell suggesting that the antisera labelled distinct populations. 3. Electrophysiological investigations were performed using an in vitro guinea-pig tracheal and bronchial preparation with intact afferent vagal pathways, including nodose and jugular ganglia. Action potentials arriving from single airway afferent nerve endings were monitored extracellularly using a glass microelectrode positioned near neuronal cell bodies in either ganglion. 4. The nodose ganglion contained the somata of mainly fast-conducting tracheal A delta fibres whereas the jugular ganglion contained equal numbers of C fibre and A delta fibre tracheal afferent somata. The nodose A delta neurones adapted rapidly to mechanical stimulation, had relatively low mechanical thresholds, were not activated by capsaicin and adapted rapidly to a hyperosmotic stimulus. By contrast, jugular A delta and C fibres adapted slowly to mechanical stimulation, were often activated by capsaicin, had higher mechanical thresholds and displayed a slow adaptation to a hyperosmotic stimulus. 5. The anatomical, physiological and pharmacological data provide evidence to support the contention that the vagal ganglionic source of the fibre supplying the airways ultimately dictates its neurochemical and physiological phenotype.
Johns Hopkins Asthma and Allergy Center, Baltimore, MD 21224, USA.
M M
MM
Ricco
W
W
Kummer
B
B
Biglari
A C
AC
Myers
B J
BJ
Undem
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D004594:Electrophysiology; D006168:Guinea Pigs; D007150:Immunohistochemistry; D009412:Nerve Fibers / Q000378:metabolism / Q000502:physiology*; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D016900:Neurofilament Proteins / Q000378:metabolism; D009475:Neurons, Afferent / Q000378:metabolism / Q000502:physiology*; D009620:Nodose Ganglion / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D018408:Patch-Clamp Techniques; D010641:Phenotype; D010812:Physical Stimulation; D017729:Presynaptic Terminals / Q000187:drug effects / Q000502:physiology; D013268:Stimulation, Chemical; D013373:Substance P / Q000378:metabolism; D014132:Trachea / Q000294:innervation / Q000502:physiology; D014630:Vagus Nerve / Q000166:cytology / Q000378:metabolism / Q000502:physiology*
D016900:Neurofilament Proteins; D013373:Substance P