Metabolic mapping of neural pathways involved in gastrosecretory response to insulin hypoglycaemia in the rat

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Abstract
The central nervous structures involved in the gastrosecretory effect of insulin hypoglycemia were investigated in 20 urethane-anesthetized rats, previously provided with a chronic gastric fistula, by means of the 2-deoxy-D-[14C]glucose autoradiographic technique. Gastric secretion increased in animals in which plasma glucose concentration was reduced to a range of 84-133 mg/100 ml. (mean .+-. SE of mean, 94 .+-. 3) as compared to a range of 125-215 mg/100 ml. (mean .+-. SE of mean, 162 .+-. 8) in animals with normal gastric secretion. In 14 of 19 structures examined, the rate of glucose utilization remained constant over the range of plasma glucose concentrations of 84-215 mg/100 ml. These structures included the ventromedial nucleus of the hypothalamus, the mamillary nuclei, the medial geniculate nuclei, globus pallidus, zona increta, nucleus ambiguus, supraoptic nucleus, paraventricular nucleus, medial nucleus of the solitary tract, dorsal tegmental nucleus, red nucleus, inferior olivary nucleus, hippocampus and amygdaloid complex. A significant inverse correlation between plasma glucose concentration and the glucose consumption rate was found in the lateral nucleus of the solitary tract, dorsal nucleus of the vagus, perifornical area where fibers of the medial forebrain bundle course, the superior olivary nucleus and the interstitial nucleus of the stria terminalis. Except for the superior olivary nucleus and the interstitial nucleus of the stria terminalis, all the structures affected by low plasma glucose concentration were previously shown to participate in the gastrosecretory response to blockade of glucose utilization by pharmacological doses of 2-deoxy-D-glucose, indicating that these same nuclei apparently are also activated by hypoglycemia.