Fore- and hindbrain mediation of gastric hypoacidity after intracerebral bombesin

Abstract

Three experiments assessed possible roles of the rat forebrain and hindbrain in the mediation of the gastric hypoacidity induced by intracerebrally administered bombesin. Experiment 1 found that bilateral electrolytic destruction of the paraventricular nucleus of the hypothalamus, which contains numerous bombesin receptors and which is immediately adjacent to the ventricular system, did not alter gastric hypoacidity after intracisternally administered bombesin (500 ng). Experiment 2, done in rats with complete coronal transections of the brain at the superior colliculus, showed that no forebrain structure is absolutely required for intracisternally administered bombesin (0, 30, 100, or 300 ng) to inhibit gastric acid secretion. Experiment 3 determined that bombesin infusions (500 ng) restricted to either the forebrain or the hindbrain by aqueductal plugs are equally effective in inhibiting acid secretion. In sum, these data suggest that both forebrain and hindbrain mechanisms exist that can mediate the inhibition of acid secretion by intracranially administered bombesin; the hindbrain mechanism does not require the forebrain to produce its effect; and lesions of forebrain structures cannot be expected to block bombesin-induced hypoacidity if bombesin reaches the hindbrain.