The majority of airway sensory innervation originates from afferent neurons whose somata reside in vagal (nodose and jugular) ganglia. Using @entity840 immunized with @entity1573 ovalbumin, we have discovered that airway @entity32 provokes phenotypic changes in the @entity4756 responsiveness of nodose neurons. Bath application of substance @entity10133 ; 0.1 to 10 microM) to nodose neurons isolated from @entity840 with normal uninflamed airways did not elicit measurable changes in resting electrophysiological properties. In sharp contrast, 80% of nodose neurons isolated 24 h after in vivo aerosolized antigen challenge of the airway were depolarized by 100 nM SP. Inhalation of a nonantigenic protein did not evoke the expression of SP responses. Pharmacological analysis revealed that SP responses unmasked by airway @entity32 were mediated by neurokinin-2 ( @entity10125 ) @entity4756 receptors. There are several potential mechanisms for transduction of an "unmasking signal" from the inflamed airway to vagal afferent somata. The vagus nerve may relay the signal, either through anterograde transport and/or nerve impulse activity. Alternatively, a signal generated by airway @entity32 may be carried by the circulation to the nodose ganglia. Unilateral vagotomy significantly reduced the percentage of SP-responsive neurons compared with intact controls, suggesting that the vagus nerve is required for unmasking of @entity10125 responses.

Antigen inhalation unmasks XXXX @entity4756 receptor-mediated responses in vagal afferents.

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity10133 :: ('2155', 'Species') :: ['P (SP'] @entity840 :: ('10141', 'Species') :: ['guinea pigs'] @entity1573 :: ('9031', 'Species') :: ['chick'] @entity10125 :: ('MESH:C006007', 'Chemical') :: ['NK-2'] @entity4756 :: ('MESH:D015320', 'Chemical') :: ['tachykinin']
@entity10125 :: (MESH:C006007,Chemical) :: ['NK-2']
