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• W1608228045 abstract "We addressed the mechanism by which antigen contracts trachea isolated from actively sensitized mice. Trachea were isolated from mice (C57BL/6J) that had been actively sensitized to ovalbumin (OVA). OVA (10 μg ml −1 ) caused histamine release (∼70% total tissue content), and smooth muscle contraction that was rapid in onset and short‐lived ( t 1/2 < 1 min), reaching approximately 25% of the maximum tissue response. OVA contraction was mimicked by 5‐HT, and responses to both OVA and 5‐HT were sensitive to 10 μ m ‐ketanserin (5‐HT 2 receptor antagonist) and strongly inhibited by atropine (1 μ m ). Epithelial denudation had no effect on the OVA‐induced contraction. Histological assessment revealed about five mast cells/tracheal section the vast majority of which contained 5‐HT. There were virtually no mast cells in the mast cell‐deficient ( sash −/−) mouse trachea. OVA failed to elicit histamine release or contractile responses in trachea isolated from sensitized mast cell‐deficient ( sash −/−) mice. Intracellular recordings of the membrane potential of parasympathetic neurons in mouse tracheal ganglia revealed a ketanserin‐sensitive 5‐HT‐induced depolarization and similar depolarization in response to OVA challenge. These data support the hypothesis that antigen‐induced contraction of mouse trachea is epithelium‐independent, and requires mast cell‐derived 5‐HT to activate 5‐HT 2 receptors on parasympathetic cholinergic neurons. This leads to acetylcholine release from nerve terminals, and airway smooth muscle contraction." @default.
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• W1608228045 date "2009-06-30" @default.
• W1608228045 modified "2023-10-16" @default.
• W1608228045 title "Mast cell-cholinergic nerve interaction in mouse airways" @default.
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• W1608228045 doi "https://doi.org/10.1113/jphysiol.2009.173054" @default.
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