Selected Publication:
SHR
Neuro
Cancer
Cardio
Lipid
Metab
Microb
Holzer, P; Danzer, M; Schicho, R; Samberger, C; Painsipp, E; Lippe, IT.
Vagal afferent input from the acid-challenged rat stomach to the brainstem: enhancement by interleukin-1beta.
NEUROSCIENCE. 2004; 129(2): 439-445.
Doi: 10.1016/j.neuroscience.2004.07.040
Web of Science
PubMed
FullText
FullText_MUG
Google Scholar
- Leading authors Med Uni Graz
-
Holzer Peter
- Co-authors Med Uni Graz
-
Lippe Irmgard Theresia
-
Meindl Claudia
-
Schicho Rudolf
-
Singewald Evelin
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Exposure of the gastric mucosa to back-diffusing concentrations of HCl (0.25 M, pH 0.51) stimulates vagal afferent input to the brainstem. Here we have examined whether pretreatment of rats with the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha causes sensitization of vagal afferent pathways to HCl. Rats were pretreated i.p. with interleukin-1beta, tumor necrosis factor-alpha (10 microg/kg) or their vehicle (sterile saline) 24, 48 and 96 h before intragastric administration of HCl (0.25 M, 1 ml/100 g). Activation of neurons in the nucleus tractus solitarii was visualized by c-Fos immunohistochemistry 2 h after the HCl challenge. I.p. administration of interleukin-1beta and tumor necrosis factor-alpha alone induced c-Fos in the brainstem, an effect that was gone after 24 h. At this time, however, the effect of HCl to cause expression of c-Fos in the nucleus tractus solitarii was significantly enhanced by pretreatment with interleukin-1beta and tumor necrosis factor-alpha. The sensitizing effect of i.p.-administered interleukin-1beta was sustained for more than 48 h and prevented by the interleukin-1 receptor antagonist anakinra. Intracisternal administration of interleukin-1beta and tumor necrosis factor-alpha (100 ng) failed to amplify the HCl-evoked expression of c-Fos in the brainstem. These results show that peripheral administration of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha induces prolonged sensitization of vagal afferent pathways to gastric HCl challenge. This effect seems to arise from a peripheral action on vagal afferents and may be of relevance to gastric chemonociception.
- Find related publications in this database (using NLM MeSH Indexing)
-
Afferent Pathways - physiology
-
Animals -
-
Brain Stem - physiology
-
Cisterna Magna -
-
Female -
-
Gastric Mucosa - drug effects Gastric Mucosa - physiology
-
Hydrochloric Acid - pharmacology
-
Immunohistochemistry -
-
Injections -
-
Injections, Intraperitoneal -
-
Interleukin 1 Receptor Antagonist Protein -
-
Interleukin-1 - administration and dosage Interleukin-1 - pharmacology
-
Interleukin-6 - administration and dosage Interleukin-6 - pharmacology
-
Intubation, Gastrointestinal -
-
Proto-Oncogene Proteins c-fos - biosynthesis Proto-Oncogene Proteins c-fos - genetics
-
Rats -
-
Rats, Sprague-Dawley -
-
Receptors, Interleukin-1 - antagonists and inhibitors
-
Sialoglycoproteins - administration and dosage Sialoglycoproteins - pharmacology
-
Tumor Necrosis Factor-alpha - administration and dosage Tumor Necrosis Factor-alpha - pharmacology
-
Vagus Nerve - physiology
- Find related publications in this database (Keywords)
-
acid insult
-
gastric mucosa
-
expression of c-Fos
-
nucleus tractus solitarii
-
proinflammatory cytokines
-
sensitization of vagal afferent pathways