Amygdaloid lesions attenuate neurogenic gastric mucosal erosions but do not alter gastric secretory changes induced by intracisternal bombesin.
Bilateral lesions of the lateral hypothalamus in rats produce glandular gastric mucosal damage. The results of the first experiment demonstrated that the severity of the neurogenic gastric erosions is attenuated by prior lesions of the centromedial amygdala. In a second experiment it was shown that fasting gastric acidity is significantly reduced following chronic amygdaloid lesions and this may be the mechanism involved in the protective nature of the amygdaloid lesions against gastric mucosal damage. In addition, it was found that gastric secretory changes induced by intracisternal injection of bombesin are unaffected by amygdaloid damage. The present results are consistent with the view that the centromedial amygdaloid region may influence gastric functions by modulating the activity of the preoptic-anterolateral hypothalamic areas or by directly influencing lower brain stem autonomic control areas.
D000679:Amygdala / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001839:Bombesin / Q000008:administration & dosage / Q000494:pharmacology*; D004572:Electrolysis; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000294:innervation / Q000378:metabolism / Q000473:pathology*; D005755:Gastrins / Q000378:metabolism; D007026:Hypothalamic Area, Lateral / Q000502:physiology; D008297:Male; D009409:Nerve Crush; D051381:Rats; D011919:Rats, Inbred Strains; D013238:Stereotaxic Techniques
D005755:Gastrins; D001839:Bombesin