Gastric acid secretion caused by gastrin-17 injection into both sides of the hypothalamic paraventricular nucleus in rats

Neuropeptides ◽  
1995 ◽  
Vol 28 (1) ◽  
pp. 13-19
Author(s):  
T Sakaguchi ◽  
T Aono ◽  
N Sandoh
1987 ◽  
Vol 252 (5) ◽  
pp. G675-G684 ◽  
Author(s):  
M. W. Gunion ◽  
Y. Tache

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.


1992 ◽  
Vol 263 (3) ◽  
pp. G414-G418 ◽  
Author(s):  
E. Saperas ◽  
H. Yang ◽  
Y. Tache

It has been established that interleukin-1 beta (IL-1 beta) injected into the cerebrospinal fluid inhibits gastric acid secretion in rats. Brain sites of action of IL-1 beta were investigated in conscious rats implanted unilaterally with chronic hypothalamic cannula. Gastric acid secretion was monitored 2 h after pylorus ligation. Human recombinant IL-1 beta (10 ng) microinjected into the medial preoptic area, anterior hypothalamus, and paraventricular nucleus inhibited gastric acid secretion by 76-83%. IL-1 beta microinjected into the ventromedial hypothalamus and other hypothalamic sites outside of responsive sites had no effect. IL-1 beta inhibitory action in the medial preoptic area was dose related (0.1-10 ng), prevented by indomethacin (5 mg/kg ip), and mimicked by prostaglandin E2. These results show that IL-1 beta acts in the medial preoptic area/anterior hypothalamus and paraventricular nucleus to inhibit acid secretion in pylorus-ligated rats and that IL-1 beta action is likely to involve prostaglandin E2.


2022 ◽  
Vol 12 ◽  
Author(s):  
Chenyu Li ◽  
Hongzhao Sun ◽  
Yuan Shi ◽  
Yan Yu ◽  
Xiaofeng Ji ◽  
...  

Background: Hydrogen sulfide (H2S) is a new type of gas neurotransmitter discovered in recent years. It plays an important role in various physiological activities. The hypothalamus paraventricular nucleus (PVN) is an important nucleus that regulates gastric function. This study aimed to clarify the role of H2S in the paraventricular nucleus of the hypothalamus on the gastric function of rats.Methods: An immunofluorescence histochemistry double-labelling technique was used to determine whether cystathionine-beta-synthase (CBS) and c-Fos neurons are involved in PVN stress. Through microinjection of different concentrations of NaHS, physiological saline (PS), D-2-Amino-5-phosphonovaleric acid (D-AP5), and pyrrolidine dithiocarbamate (PDTC), we observed gastric motility and gastric acid secretion.Results: c-Fos and CBS co-expressed the most positive neurons after 1 h of restraint and immersion, followed by 3 h, and the least was at 0 h. After injection of different concentrations of NaHS into the PVN, gastric motility and gastric acid secretion in rats were significantly inhibited and promoted, respectively (p < 0.01); however, injection of normal saline, D-AP5, and PDTC did not cause any significant change (p > 0.05). The suppressive effect of NaHS on gastrointestinal motility and the promotional effect of NaHS on gastric acid secretion could be prevented by D-AP5, a specific N-methyl-D-aspartic acid (NMDA) receptor antagonist, and PDTC, an NF-κB inhibitor.Conclusion: There are neurons co-expressing CBS and c-Fos in the PVN, and the injection of NaHS into the PVN can inhibit gastric motility and promote gastric acid secretion in rats. This effect may be mediated by NMDA receptors and the NF-κB signalling pathway.


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