title: Response properties of the brainstem neurons of the cat following intra-esophageal acid-pepsin infusion.
abstract: Studies in humans have documented that acute acid infusion into the esophagus leads to decrease in threshold for sensations to mechanical distension of the esophagus. It is not known whether acid infusion leads to sensitization of brainstem neurons receiving synaptic input from vagal afferent fibers innervating the esophagus. The aim of this study was to investigate the correlation of responses of vagal afferents and brainstem neurons after acute infusion of acid (0.1 N HCl)+pepsin (1 mg/ml) into the esophagus of cats. The vagal afferent fibers (n=20) exhibited pressure-dependent increase in firing to graded esophageal distension (5-80 mm Hg). Infusion of acid+pepsin into the esophagus produced a significant increase in ongoing resting firing of five of 16 fibers (31%) tested. However, their responses to graded esophageal distension did not change when tested 30 min after infusion. Pepsin infusion did not change the resting firing and response to esophageal distension (n=4). Twenty-one brainstem neurons were recorded that responded in an intensity-dependent manner to graded esophageal distension. Responses of 12 excited neurons were tested after intra-esophageal acid+pepsin infusion. Neurons exhibited a decrease in threshold for response to esophageal distension and increase in firing after acid+pepsin infusion. The sensitization of response after intra-esophageal acid remained unaffected after cervical (C1-C2) spinal transection (n=3). Results indicate that the esophageal distension-sensitive neurons in the brainstem exhibit sensitization of response to esophageal distension after acute acid+pepsin exposure. The sensitization of brainstem neurons is possibly initiated by increased spontaneous firing of the vagal afferent fibers to acid+pepsin, but not to sensitized response of vagal distension-sensitive afferent fibers to esophageal distension. Results also indicate that spinal pathway does not contribute to sensitization of brainstem neurons.
authors.affiliation: MCW Dysphagia Institute and Division of Gastroenterology and Hepatology, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226, USA.
authors.forename: B K
authors.initials: BK
authors.lastname: Medda
authors.forename: J N
authors.initials: JN
authors.lastname: Sengupta
authors.forename: I M
authors.initials: IM
authors.lastname: Lang
authors.forename: R
authors.initials: R
authors.lastname: Shaker
mesh_terms: D000818:Animals; D001933:Brain Stem / Q000502:physiology*; D002415:Cats; D004106:Dilatation; D004594:Electrophysiology; D004947:Esophagus / Q000294:innervation*; D005260:Female; D006851:Hydrochloric Acid / Q000494:pharmacology*; D008297:Male; D008465:Mechanoreceptors / Q000187:drug effects / Q000502:physiology; D008839:Microelectrodes; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D010434:Pepsin A / Q000494:pharmacology*; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology; D017833:Visceral Afferents / Q000187:drug effects / Q000502:physiology
chemical_list: D010434:Pepsin A; D006851:Hydrochloric Acid