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Afferent convergence of noxious pulmonary input onto T9‐T10 spinal neurons responding to gastric distension in rats
Author(s) -
Farber Jay P,
Qin Chao,
Foreman Robert D
Publication year - 2006
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.20.4.a374-a
Subject(s) - gastric distension , distension , noxious stimulus , medicine , neuroscience , nociception , biology , receptor
In the spinal cord, afferent‐afferent neuronal cross‐talk among visceral organs has been suggested as a neural mechanism contributing to visceroviceral hypersensitivity. The aim of the present study is to determine whether irritation of the lungs can affect activity of T9–T10 spinal neurons receiving input from the stomach. Extracellular potentials of T9–T10 spinal neurons receiving gastric input were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. Lower airways were irritated using ammonia vapor over a 30% NH 4 OH solution (0.5, 1.0 ml), injected into inspiratory line of the ventilator over 20 s. Gastric distension (GD, 20, 60 mmHg, 20 s) was performed by air inflation of a balloon in the stomach. Inhaled ammonia (IA) altered activity of 29/43 (67%) spinal neurons responding to GD. Of the deeper neurons tested (depth: 0.3–1.2 mm), 20/31 neurons responded with excitatory (E, n=12), inhibitory (I, n=7) or biphasic patterns (E‐I, n=1), whereas 7/12 superficial neurons (depth < 0.3 mm) with GD‐input were suppressed by IA and 2 neurons were excited. Bilateral cervical vagotomy abolished responses to IA in 2/7 tested neurons (2I), but 5 neurons (2E, 3I) had spinal inputs. Desensitization of vanilloid receptor‐1 containing neurons using resiniferatoxin (2.0 μg/kg, i.v.) abolished responses to IA in 3/3 neurons (2I, 1E). These results showed that irritation of lower airways affected activity in T9–T10 spinal neurons receiving gastric input. Vagal and spinal sympathetic afferent fibers containing vanilloid receptor‐1 contribute to viscerovisceral cross‐talk between lungs and stomach. (Supported by NS‐35471, HL‐075524)