Fore- and hindbrain mediation of gastric hypoacidity after intracerebral bombesin

1987 ◽  
Vol 252 (5) ◽  
pp. G675-G684 ◽  
Author(s):  
M. W. Gunion ◽  
Y. Tache
Keyword(s):  
Superior Colliculus ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Ventricular System ◽  
Rat Forebrain ◽  
The Brain ◽  
Bombesin Receptors

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.

Hepatic modulation of insulin-induced gastric acid secretion and EMG activity in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R346-R352 ◽  
Author(s):  
J. Granneman ◽  
M. I. Friedman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Emg Activity ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Inhibited Acid ◽  
Hepatic Portal ◽  
The Brain

Intravenous infusions of fructose, a hexose that does not cross the blood-brain barrier, suppressed insulin-induced gastric acid secretion and electromyographic (EMG) activity despite continuing hypoglycemia. Hepatic portal vein infusions of 0.15 M fructose inhibited acid output while the same concentration delivered via the jugular vein did not, suggesting a hepatic site of action of the hexose. Only infusions of fructose that began before onset of the insulin-induced gastric responses were effective, whereas glucose infusions, which elevated plasma glucose levels, readily reversed ongoing gastric activity. The suppressive effects of fructose on gastric activity were prevented by prior section of the hepatic branch of the vagus nerve. In contrast, hepatic vagotomy did not prevent suppression of gastric responses by infusions of glucose, a hexose utilized by both brain and liver. These results suggest that receptors in the brain may initiate and terminate insulin-induced gastric acid secretion and motor activity, whereas sensors in the liver may inhibit these responses.

scholarly journals Cocaine-Amphetamine-Regulated Transcript (CART) Acts in the Central Nervous System to Inhibit Gastric Acid Secretion via Brain Corticotropin-Releasing Factor System*

Endocrinology ◽  
2000 ◽  
Vol 141 (8) ◽  
pp. 2854-2860 ◽  
Author(s):  
Toshikatsu Okumura ◽  
Hiroto Yamada ◽  
Wataru Motomura ◽  
Yutaka Kohgo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Inhibition ◽  
Gastric Function ◽  
The Central Nervous System ◽  
The Brain

Recent study has indicated that cocaine-amphetamine-regulated transcript (CART) is an anorectic chemical in the brain. In the present study, we examined the hypothesis that CART may act in the central nervous system to alter gastric function. Food consumption, gastric acid secretion, and gastric emptying were measured after injection of CART into the cerebrospinal fluid in 24-h fasted Sprague Dawley rats. Central injection of CART inhibited food intake, gastric acid secretion, and gastric emptying. In contrast, ip injection of CART failed to inhibit gastric acid secretion and gastric emptying, suggesting that CART acts in the brain to suppress gastric acid secretion and gastric emptying. In the vagotomized animals, centrally administered CART did inhibit pentagastrin-stimulated gastric acid secretion. The CART-induced acid inhibition was also observed in rats treated with indomethacin, a cyclooxygenase inhibitor. In contrast, pretreatment with central administration of a CRF receptor antagonist,α -helical CRF9–41, completely blocked the central CART-induced inhibition of gastric acid secretion. All these results suggest that CART acts in the brain to inhibit gastric function via brain CRF system. The vagal pathway and the prostaglandin system are not involved in the acid inhibition.

scholarly journals Peripheral PYY inhibits intracisternal TRH-induced gastric acid secretion by acting in the brain

2000 ◽  
Vol 279 (3) ◽  
pp. G575-G581 ◽  
Author(s):  
Hong Yang ◽  
Keishi Kawakubo ◽  
Helen Wong ◽  
Gordon Ohning ◽  
John Walsh ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Supporting Evidence ◽  
Intracisternal Injection ◽  
Site Of Action ◽  
The Brain

The site of action of peripheral peptide YY (PYY)-induced inhibition of vagally stimulated gastric acid secretion was studied using immunoneutralization with PYY antibody in urethan-anesthetized rats. Gastric acid secretion (59 ± 7 μmol/90 min) stimulated by intracisternal injection of the stable thyrotropin-releasing hormone (TRH) analog RX-77368 (14 pmol/rat) was dose-dependently inhibited by 52%, 69%, and 83% by intravenous infusion of 0.25, 0.5, and 1.0 nmol · kg−1 · h−1 PYY, respectively. PYY or PYY3–36 (2.4 pmol/rat) injected intracisternally also inhibited the acid response to intracisternal RX-77368 by 73% and 80%, respectively. Intravenous pretreatment with PYY antibody (4.5 mg/rat), which shows a 35% cross-reaction with PYY3–36 by RIA, completely prevented the inhibitory effect of intravenously infused PYY (1 nmol · kg−1 · h−1). When injected intracisternally, the PYY antibody (280 μg/rat) reversed intracisternal PYY (2.4 pmol)- and intravenous PYY (1 nmol · kg−1 · h−1)-induced inhibition of acid response to intracisternal RX-77368 by 64% and 93.5%, respectively. These results provide supporting evidence that peripheral PYY inhibits central vagal stimulation of gastric acid secretion through an action in the brain.

Interleukin-1 beta acts at hypothalamic sites to inhibit gastric acid secretion in rats

1992 ◽  
Vol 263 (3) ◽  
pp. G414-G418 ◽  
Author(s):  
E. Saperas ◽  
H. Yang ◽  
Y. Tache
Keyword(s):  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Medial Preoptic Area ◽  
Anterior Hypothalamus ◽  
Interleukin 1 Beta

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.

scholarly journals Effects of Exogenous Hydrogen Sulfide in the Hypothalamic Paraventricular Nucleus on Gastric Function in Rats

2022 ◽  
Vol 12 ◽  
Author(s):  
Chenyu Li ◽  
Hongzhao Sun ◽  
Yuan Shi ◽  
Yan Yu ◽  
Xiaofeng Ji ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Gastric Motility ◽  
Physiological Saline ◽  
Pyrrolidine Dithiocarbamate ◽  
Double Labelling ◽  
Gastric Function

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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