Immunocytochemical characterization of rat brainstem neurons with vagal afferent input from the stomach challenged by acid or ammonia

Exposure of the gastric mucosa to backdiffusing acid is signalled to the brainstem via vagal afferents. This study examined whether exposure of the Sprague-Dawley rat stomach to hydrochloric acid (HCl) or ammonium hydroxide (NH(4)OH), a noxious chemical produced by Helicobacter pylori activates different vagal afferent pathways as reflected by different circuitries in the medullary brainstem. Two hours after intragastric treatment with HCl or NH(4)OH the activation of neurons in the nucleus tractus solitarii at the rostrocaudal extension of the area postrema (NTS(AP)) was visualized by c-Fos immunohistochemistry and their chemical coding characterized by double-labelling immunohistochemistry. Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH(4)OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS(AP) The number and distribution of NTS(AP) neurons activated by 0.35 M HCl and 0.3 M NH(4)OH were similar; the highest number of activated neurons occurring in the medial part of the NTS(AP) Some 60% of the NTS(AP) neurons activated by intragastric HCl and NH(4)OH stained for the high affinity glutamate transporter EAAC1, while some 30% contained calbindin or neuropeptide Y Glutamate receptors of the N-methyl-D-aspartate type were found on approximately 50% of the c-Fos-positive cells in the NTS(AP), whereas tachykinin NK(1), NK(2) and NK(3) receptors were present on 5-10% of the activated neurons. The similar number and distribution of c-Fos-expressing neurons within the NTS(AP) and their identical chemical coding indicate that exposure of the rat stomach to backdiffusing concentrations of HCl and NH(4)OH activates the same vagal afferent-NTS(AP) pathway.