TNF-alpha activates solitary nucleus neurons responsive to gastric distension.
Tumor necrosis factor-alpha (TNF-alpha) is liberated as part of the immune response to antigenic challenge, carcinogenesis, and radiation therapy. Previous studies have implicated elevated circulating levels of this cytokine in the gastric hypomotility associated with these disease states. Our earlier studies suggest that a site of action of TNF-alpha may be within the medullary dorsal vagal complex. In this study, we describe the role of TNF-alpha as a neuromodulator affecting neurons in the nucleus of the solitary tract that are involved in vago-vagal reflex control of gastric motility. The results presented herein suggest that TNF-alpha may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.
Emch
G S
GS
Department of Neuroscience, College of Medicine, Ohio Sate University, Columbus, Ohio 43210, USA.
Hermann
G E
GE
Rogers
R C
RC
D000818:Animals; D004305:Dose-Response Relationship, Drug; D013271:Gastric Dilatation / Q000503:physiopathology*; D005746:Gastric Emptying / Q000502:physiology; D008297:Male; D008845:Microinjections; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D020318:Rats, Long-Evans; D012018:Reflex / Q000502:physiology; D017552:Solitary Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D013270:Stomach / Q000294:innervation* / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014630:Vagus Nerve / Q000502:physiology
D014409:Tumor Necrosis Factor-alpha