5-HT3 receptors mediate inflammation-induced unmasking of functional tachykinin responses in vitro

Author:

Moore Kimberly A.1,Oh Eun Joo1,Weinreich Daniel1

Affiliation:

1. Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201

Abstract

Exogenously applied tachykinins produce no measurable electrophysiological responses in the somata of vagal afferent neurons [nodose ganglion neurons (NGNs)] isolated from naive guinea pigs. By contrast, after in vitro antigen challenge of nodose ganglia from guinea pigs immunized with chick ovalbumin, ∼60% (53 of 89) of NGNs were depolarized an average of 13 ± 1.2 mV by substance P (SP; 100 nM; n = 53). Receptor antagonists and enzyme inhibitors were utilized to screen a number of mast cell-derived mediators for their role in the uncovering or “unmasking” of functional tachykinin receptors after antigen challenge. Two chemically distinct 5-hydroxytryptamine-3-receptor antagonists significantly reduced the percentage of NGNs displaying depolarizing SP responses. Treatment with Y-25130 (1 or 10 μM) or tropisetron (1 μM) 15 min before and during antigen challenge reduced the percentage of SP-responsive neurons to ∼20 and ∼15%, respectively. These results suggest that activation of 5-hydroxytryptamine-3 receptors plays an integral role in the unmasking of functional tachykinin receptors after specific antigen challenge of nodose ganglia. The mediator(s) underlying tachykinin-receptor unmasking in the remainder of the NGNs has yet to be characterized. However, it does not appear to be histamine, prostanoids, or peptidoleukotrienes.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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