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Bacterial Phylum Spirochaetes
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Localization of central prostaglandin E2 antisecretory effects.
E Barocelli1, M Impicciatore, J Seaton
1Division of General Surgery, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey.
Gastroenterology
|February 1, 1991
Summary
Prostaglandin E2 (PGE2) injected into specific brain regions, including the ventromedial hypothalamus and central amygdala, significantly reduces stimulated gastric acid secretion in rats. These findings suggest PGE2 plays a key role in the central regulation of stomach acid production.
Area of Science:
- Neuroscience
- Gastroenterology
- Pharmacology
Background:
- Intracerebroventricular prostaglandin E2 (PGE2) is known to inhibit gastric acid secretion, but its central site of action remains unclear.
- PGE2 receptors are present in the ventromedial hypothalamic nucleus and central amygdala, and the nucleus accumbens is implicated in neurotensin-induced antisecretory effects.
Purpose of the Study:
- To investigate the hypothesis that microinjections of PGE2 into the ventromedial hypothalamic nucleus, central amygdala, and nucleus accumbens inhibit stimulated gastric acid secretion.
- To determine the role of specific brain regions in the central control of gastric acid secretion by PGE2.
Main Methods:
- Stereotaxic surgery was used to implant cannulas into specific brain areas (ventromedial hypothalamic nucleus, central amygdala, nucleus accumbens, hippocampus) in male Sprague-Dawley rats.
- Rats were administered varying doses of PGE2 (0.1-1.0 micrograms) or saline into the brain 10 minutes before subcutaneous injection of pentagastrin.
- Gastric acid secretion was measured and expressed as acid output (micromoles per hour).
Main Results:
- Microinjections of PGE2 into the ventromedial hypothalamic nucleus, nucleus accumbens, and central amygdala dose-dependently inhibited pentagastrin-stimulated gastric acid secretion.
- The hippocampus, used as a control region, showed no significant effect of PGE2 administration on acid output.
- Central PGE2 administration induced hyperthermia, but at lower doses than those required for gastric acid inhibition.
Conclusions:
- PGE2 administration into the ventromedial hypothalamic nucleus, central amygdala, and nucleus accumbens inhibits stimulated gastric acid secretion.
- These results suggest that PGE2 has a physiological role in the central nervous system's control of gastric acid secretion.
- Specific brain regions with known PGE2 receptors are involved in this inhibitory effect.
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