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.

CNS regulation of gastric and autonomic functions in dogs by gastrin-releasing peptide

1988 ◽  
Vol 255 (3) ◽  
pp. G298-G303
Author(s):  
H. J. Lenz
Keyword(s):  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Left Gastric Artery ◽  
Gastric Artery ◽  
Ganglionic Blockade ◽  
The Central Nervous System ◽  
Artery Flow

The central nervous system effects of canine gastrin-releasing peptide (GRP) were studied on gastric acid secretion, emptying, blood flow, and the autonomic nervous system in conscious dogs. GRP injected into the third cerebral ventricle significantly (P less than 0.01) increased plasma epinephrine but not norepinephrine concentrations. GRP (0.1-1.0 nmol/kg) significantly decreased gastric acid secretion stimulated by an 8% peptone meal, delayed gastric emptying of the liquid peptone meal, and increased left gastric artery flow. Ganglionic blockade, truncal vagotomy, or adrenalectomy did not abolish the inhibitory effect of GRP on gastric acid secretion. However, ganglionic blockade or vagotomy abolished the GRP-induced inhibition of gastric emptying, and ganglionic blockade or adrenalectomy abolished the GRP-induced increases in left gastric artery flow and plasma epinephrine concentrations. An intravenous infusion of epinephrine that produced similar plasma concentrations of epinephrine that were observed after cerebroventricular injection of GRP mimicked the increase in left gastric artery flow induced by GRP. It is concluded that 1) GRP acts within the central nervous system to activate the sympathoadrenal axis, 2) GRP inhibits gastric emptying of a liquid meal by a vagally dependent mechanism and enhances left gastric artery flow by the release of epinephrine from the adrenal medulla, and 3) the pathway(s) that mediate the GRP-induced inhibition of gastric acid in the dog remain unknown.

Pathways mediating CRF-induced inhibition of gastric acid secretion in rats

1989 ◽  
Vol 256 (1) ◽  
pp. G214-G219 ◽  
Author(s):  
G. Druge ◽  
A. Raedler ◽  
H. Greten ◽  
H. J. Lenz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Concentrations ◽  
Conscious Rats ◽  
The Central Nervous System

The pathways involved in mediating the central nervous system actions of corticotropin-releasing factor (CRF) on gastric acid secretion were examined in conscious rats. CRF (0.1-2.0 nmol) given cerebroventricularly inhibited gastric acid secretion stimulated by pentagastrin (P less than 0.01). This effect was abolished by cerebroventricular but not intravenous administration of a specific CRF receptor antagonist, alpha-helical CRF-(9-41). Ganglionic blockade with chlorisondamine chloride, noradrenergic blockade with bretylium, or adrenalectomy abolished the gastric inhibitory action of CRF whereas truncal vagotomy or opiate blockade with naloxone did not. A vasopressin receptor antagonist significantly inhibited but did not abolish the gastric inhibitory action of CRF. An intravenous infusion of epinephrine that mimicked the epinephrine plasma concentrations which were observed after cerebroventricular administration of CRF did not alter pentagastrin-stimulated gastric acid secretion. These results indicate that CRF acts within the central nervous system to inhibit gastric acid secretion by a specific receptor-mediated event. Inhibition of gastric acid secretion by CRF in conscious rats is mediated by efferent fibers of the sympathetic nervous system and in part by a vasopressin-dependent pathway but not by the parasympathetic nervous system, adrenal epinephrine release, or opiate-sensitive pathways.

Ghrelin Acts in the Central Nervous System to Stimulate Gastric Acid Secretion

2001 ◽  
Vol 280 (3) ◽  
pp. 904-907 ◽  
Author(s):  
Yukari Date ◽  
Masamitsu Nakazato ◽  
Noboru Murakami ◽  
Masayasu Kojima ◽  
Kenji Kangawa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
The Central Nervous System

Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function

2006 ◽  
Vol 291 (1) ◽  
pp. G156-G162 ◽  
Author(s):  
K. L. Whited ◽  
D. Thao ◽  
K. C. Kent Lloyd ◽  
A. S. Kopin ◽  
H. E. Raybould
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Feedback Inhibition ◽  
Vagal Afferents ◽  
Afferent Pathway ◽  
Gastric Function ◽  
Vagal Afferent ◽  
Fos Expression

Cholecystokinin (CCK), acting at CCK1 receptors (CCK1Rs) on intestinal vagal afferent terminals, has been implicated in the control of gastrointestinal function and food intake. Using CCK1R−/− mice, we tested the hypothesis that lipid-induced activation of the vagal afferent pathway and intestinal feedback of gastric function is CCK1R dependent. In anesthetized CCK1R+/+ (“wild type”) mice, meal-stimulated gastric acid secretion was inhibited by intestinal lipid infusion; this was abolished in CCK1R−/− mice. Gastric emptying of whole egg, measured by nuclear scintigraphy in awake mice, was significantly faster in CCK1R−/− than CCK1R+/+ mice. Gastric emptying of chow was significantly slowed in response to administration of CCK-8 (22 pmol) in CCK1R+/+ but not CCK1R−/− mice. Activation of the vagal afferent pathway was measured by immunohistochemical localization of Fos protein in the nucleus of the solitary tract (NTS; a region where vagal afferents terminate). CCK-8 (22 pmol ip) increased neuronal Fos expression in the NTS of fasted CCK1R+/+ mice; CCK-induced Fos expression was reduced by 97% in CCK1R−/− compared with CCK1R+/+ mice. Intralipid (0.2 ml of 20% Intralipid and 0.04 g lipid), but not saline, gavage increased Fos expression in the NTS of fasted CCK1R+/+ mice; lipid-induced Fos expression was decreased by 47% in CCK1R−/− compared with CCK1R+/+mice. We conclude that intestinal lipid activates the vagal afferent pathway, decreases gastric acid secretion, and delays gastric emptying via a CCK1R-dependent mechanism. Thus, despite a relatively normal phenotype, intestinal feedback in response to lipid is severely impaired in these mice.

Neuromedin U acts in the central nervous system to inhibit gastric acid secretion via CRH system

2003 ◽  
Vol 284 (6) ◽  
pp. G963-G969 ◽  
Author(s):  
Muhtashan S. Mondal ◽  
Yukari Date ◽  
Noboru Murakami ◽  
Koji Toshinai ◽  
Takuya Shimbara ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Stress Responses ◽  
Energy Homeostasis ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Acid Inhibition ◽  
Dependent Manner ◽  
The Central Nervous System

Neuromedin U (NMU) is a hypothalamic peptide involved in energy homeostasis and stress responses. NMU, when administered intracerebroventricularly, decreases food intake and body weight while increasing body temperature and heat production. In addition, NMU, acting via the corticotropin-releasing hormone (CRH) system, induces gross locomotor activity and stress responses. We studied the effect of intracerebroventricularly administered NMU (0.5–4 nmol) in the regulation of gastric functions in conscious rats. Intracerebroventricular administration of NMU significantly decreased gastric acid output to 30–60% and gastric emptying to 35–70% in a dose-dependent manner. Vagotomy did not abolish the inhibitory effect of NMU on pentagastrin-induced gastric acid secretion. Pretreatment with indomethacin (10 mg/kg), an inhibitor of prostaglandin synthesis, also did not affect NMU-induced acid inhibition. Pretreatment with anti-CRH IgG (1 μg/rat), however, completely blocked NMU-induced acid inhibition ( P < 0.01). Administration of yohimbine (4 mg/kg), an α2-adrenergic receptor antagonist, also abolished NMU-induced acid inhibition ( P < 0.01). These findings suggest that NMU is critical in the central regulation of gastric acid secretion via CRH.

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