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. 1980;300:393–407. doi: 10.1113/jphysiol.1980.sp013168

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

Massako Kadekaro 1,*, Helen Savaki 1, Louis Sokoloff 1
PMCID: PMC1279361  PMID: 6770083

Abstract

1. The central nervous structures involved in the gastrosecretory effect of insulin hypoglycaemia were investigated in twenty urethane-anaesthetized rats, previously provided with a chronic gastric fistula, by means of the 2-deoxy-D-[14C]glucose autoradiographic technique.

2. Gastric secretion increased in animals in which plasma glucose concentration was reduced to a range of 84-133 mg/100 ml. (mean ± S.E. of mean, 94 ± 3) as compared to a range of 125-215 mg/100 ml. (mean ± S.E. of mean, 162 ± 8) in animals with normal gastric secretion.

3. In fourteen of nineteen 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 incerta, nucleus ambiguus, supraoptic nucleus, paraventricular nucleus, medial nucleus of the solitary tract, dorsal tegmental nucleus, red nucleus, inferior olivary nucleus, hippocampus and amygdaloid complex.

4. A significant inverse correlation between plasma glucose concentration and the rate of glucose consumption was found in the lateral nucleus of the solitary tract, dorsal nucleus of the vagus, perifornical area where fibres of the medial forebrain bundle course, the superior olivary nucleus and the interstitial nucleus of the stria terminalis.

5. Except for the superior olivary nucleus and the interstitial nucleus of the stria terminalis, all the structures affected by low plasma glucose concentration have previously been 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 are also activated by hypoglycaemia.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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