The role of paraventricular nucleus of hypothalamus in stress-ulcer formation in rats

Abstract

The rat stress model of restraint and cold water immersion was used to investigate the effect of stimulating the paraventricular nucleus (PVN) of hypothalamus on the development of stress-induced gastric ulceration. The results were (1) electric stimulation of the PVN increased the stress ulceration, while electrolytic lesion of the PVN decreased it; (2) intracerebroventricular injection (i.c.v.) of acetylcholine (Ach) enhanced the effect of PVN stimulation on stress ulcers, and the M-receptor was involved; (3) i.c.v. norepinephrine (NE) attenuated the effect of PVN stimulation on stress ulcers in a dose-dependent manner, and the beta-receptor was involved; (4) i.c.v. 5-hydroxytryptamine (5-HT) enhanced the effect of PVN stimulation on stress ulcers; (5) electrolytic lesions of dorsal raphe nucleus (DR) attenuated the effect of PVN stimulation on stress ulcers, while electrolytic lesions of the locus ceruleus (LC) aggravated the effect; (6) thyroidectomy, adrenalectomy, ovariectomy, vagotomy and sympathectomy all attenuated the effect of PVN stimulation on stress ulcers; (7) electric stimulation of the PVN produced no effect on gastric juice volume, acidity, total acid output, pepsin activity or the gastric barrier mucus; but greatly reduced gastric mucosal blood flow. These results indicate that the PVN is an important brain site regulating the development of stress-induced gastric ulcers, that the classical neurotransmitters Ach, NE and 5-HT are involved, and that in the periphery, both the parasympathetic and sympathetic nervous systems and the three endocrine glands (thyroid, adrenal and gonad) take part in the effect.