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. Pre vious studies have implicated elevated circulating levels of this cytokine in the gastric hypomotility associated with these disease states. Our earli er studies suggest that a site of action of TNF-alpha may be within the med ullary dorsal vagal complex. In this study, we describe the role of TNF-alp ha as a neuromodulator affecting neurons in the nucleus of the solitary tra ct that are involved in vago-vagal reflex control of gastric motility. The results presented herein suggest that TNF-alpha may induce a persistent gas tric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.