Lateral Hypothalamic Mediation of Hypergastrinemia Induced by Intracisternal Bombesin

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Abstract
Electrolytic lesions of the lateral hypothalamus (LH), but not of the lateral thalamus, prevented the elevation of serum gastrin induced by intracisternal injection of bombesin in rats. Knife cuts through the lateral or the posterior LH border largely abolished the rise in circulating gastrin induced by intracisternal bombesin. Cuts through the media LH border partly inhibited the response; cuts through the anterior LH border did not modify peptide action. None of the transections altered basal gastrin levels nor the rise in gastric pH and inhibition of gastric acid output induced by intracisternal bombesin. LH lesions did not modify the rise in serum gastrin induced by i.v. bombesin. The gastrin-releasing effect of intracisternal bombesin requires the integrity of fibers crossing the posterior, lateral, and medial borders of the LH and is independent of changes in gastric pH. The LH area is not itself necessary for the expression of the inhibitory action of bombesin on gastric acid secretion.