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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
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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.

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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.