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Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Danzer, M; Jocic, M; Samberger, C; Painsipp, E; Bock, E; Pabst, MA; Crailsheim, K; Schicho, R; Lippe, IT; Holzer, P.
Stomach-brain communication by vagal afferents in response to luminal acid backdiffusion, gastrin, and gastric acid secretion.
AMER J PHYSIOL-GASTROINTEST L. 2004; 286(3): G403-G411.
Doi: 10.1152/ajpgi.00308.2003
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- Leading authors Med Uni Graz
- Holzer Peter
- Co-authors Med Uni Graz
- Bock Elisabeth
- Lippe Irmgard Theresia
- Meindl Claudia
- Pabst Maria-Anna
- Schicho Rudolf
- Singewald Evelin
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- Abstract:
- Vagal afferents play a role in gut-brain signaling of physiological and pathological stimuli. Here, we investigated how backdiffusion of luminal HCl or NH(4)OH and pentagastrin-stimulated acid secretion interact in the communication between rat stomach and brain stem. Rats were pretreated intraperitoneally with vehicle or appropriate doses of cimetidine, omeprazole, pentagastrin, dexloxiglumide (CCK(1) receptor antagonist), and itriglumide (CCK(2) receptor antagonist) before intragastric administration of saline or backdiffusing concentrations of HCl or NH(4)OH. Two hours later, neuronal activation in the nucleus of the solitary tract (NTS) and area postrema was visualized by c-Fos 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, which was not related to gender, gastric mucosal injury, or gastropyloric motor alterations. The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide. Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide. We conclude that vagal afferents transmit physiological stimuli (gastrin) and pathological events (backdiffusion of luminal HCl or NH(4)OH) from the stomach to the brain stem. These communication modalities interact because, firstly, acid secretion enhances afferent signaling of gastric acid backdiffusion and, secondly, gastrin activates NTS neurons through stimulation of CCK(1) receptors on vagal afferents and of CCK(2) receptors on area postrema neurons projecting to the NTS.
- Find related publications in this database (using NLM MeSH Indexing)
- Afferent Pathways - physiology
- Ammonia - pharmacology
- Animals -
- Anti-Ulcer Agents - pharmacology
- Autoradiography -
- Brain - physiology
- Brain Stem - physiology
- Diffusion -
- Female -
- Gastric Acid - secretion
- Gastrins - secretion
- Gastrointestinal Motility - physiology
- Gene Expression - drug effects
- Genes, fos - genetics
- In Situ Hybridization -
- Male -
- Neurons - physiology
- Pentagastrin - pharmacology
- Pressure -
- RNA, Messenger - biosynthesis
- Rats -
- Rats, Sprague-Dawley -
- Receptors, Cholecystokinin - antagonists and inhibitors Receptors, Cholecystokinin - metabolism
- Sex Characteristics -
- Solitary Nucleus - metabolism
- Spinal Cord - physiology
- Stomach - physiology
- Vagus Nerve - physiology
- Find related publications in this database (Keywords)
- ammonium hydroxide
- gastropyloric motility
- expression of c-Fos in the nucleus of the solitary tract