Reflex Effects of Oral, Gastrointestinal and Hepatoportal Glutamate Sensors on Vagal Nerve Activity

Abstract

Glutamate sensors in the oral cavity, gastrointestinal canal and hepatoportal region are thought to function in the reflex regulation of vagal activity to the gastrointestinal tract and pancreas. In support of this notion, the findings summarized in this report demonstrate that the infusion of monosodium glutamate (MSG) into the stomach (150 mmol/L, 3 mL), duodenum (150 mmol/L, 3 mL) and portal vein (10 mmol/L, 0.1 mL) increases afferent activity in the vagal gastric, celiac and hepatic nerves, suggesting the existence of glutamate sensors in the gastric wall, intestinal wall and hepatoportal region. Further, oral, gastric and intestinal infusions of MSG (150 mmol/L, isotonic solution) and the infusion of MSG (10 mmol/L, 0.1 mL) into the portal vein resulted in reflex activation of the efferent gastric and pancreatic branches of the vagus. The intravenous injection of 10 mmol/L MSG (0.1 mL) also induced a reflex activation of the efferent discharges of the gastric branch of the vagus; however, in hepatic and celiac vagotomized rats, the intravenous injection of MSG (1 or 3mol/L, 1 mL) produced no effect on gastric vagal activity. The results of these experiments demonstrate the importance of the afferent nerve signals from visceral glutamate sensors in generating the reflex activation of gastrointestinal and pancreatic functions in response to MSG administration.