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activates solitary nucleus
neurons responsive to gastric distension
Department of Neuroscience, College of Medicine, Ohio Sate University, Columbus, Ohio 43210
Tumor necrosis factor-
(TNF-) 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- may be within the medullary dorsal vagal complex. In this study, we describe the role of TNF- 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- may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.
cytokines; brain; gastric motility; tumor necrosis factor-
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