Excitation of neurons in the medullary raphe increases gastric acid and pepsin production in cats

White, RD; Rossiter, C. D.; Hornby, Pamela J.; Harmon, John W.; Kasbekar, D. K.; Gillis, Richard A.

doi:10.1152/ajpgi.1991.260.1.g91

Cited by 13 publications

(12 citation statements)

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“…Activation of the caudal raphe nuclei increases gastric pepsin secretion in anesthetized animals in a vagally dependent manner (535). Similarly, stimulation of the DVC induces gastric prostaglandin release, which appears to play a significant role in gastric mucosal protection in response to stress (43, 107, 459).…”

Section: Vagal Efferent Motoneuronsmentioning

confidence: 99%

“…Microinjection of TRH into the DVC increases gastric motility and acid secretion in a vagally dependent manner (221, 452, 463, 535). Additionally, activation of neurons within the raphe pallidus, raphe obscurus, or parapyramidal regions induces a vagally dependent increase in gastric acid secretion that is attenuated by pretreatment with DVC microinjection of a TRH antibody (176, 222).…”

Section: Cns Regulation Of Sympathetic and Parasympathetic Control Ofmentioning

confidence: 99%

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Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Browning

Travagli

2014

Comprehensive Physiology

433

388

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Although the gastrointestinal (GI) tract possesses intrinsic neural plexuses that allow a significant degree of autonomy over GI functions, the central nervous system (CNS) provides extrinsic neural inputs that regulate, modulate, and control these functions. While the intestines are capable of functioning in the absence of extrinsic inputs, the stomach and esophagus are much more dependent upon extrinsic neural inputs, particularly from parasympathetic and sympathetic pathways. The sympathetic nervous system exerts a predominantly inhibitory effect upon GI muscle and provides a tonic inhibitory influence over mucosal secretion while, at the same time, regulates GI blood flow via neurally mediated vasoconstriction. The parasympathetic nervous system, in contrast, exerts both excitatory and inhibitory control over gastric and intestinal tone and motility. Although GI functions are controlled by the autonomic nervous system and occur, by and large, independently of conscious perception, it is clear that the higher CNS centers influence homeostatic control as well as cognitive and behavioral functions. This review will describe the basic neural circuitry of extrinsic inputs to the GI tract as well as the major CNS nuclei that innervate and modulate the activity of these pathways. The role of CNS-centered reflexes in the regulation of GI functions will be discussed as will modulation of these reflexes under both physiological and pathophysiological conditions. Finally, future directions within the field will be discussed in terms of important questions that remain to be resolved and advances in technology that may help provide these answers.

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Section: Vagal Efferent Motoneuronsmentioning

confidence: 99%

Section: Cns Regulation Of Sympathetic and Parasympathetic Control Ofmentioning

confidence: 99%

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Browning

Travagli

2014

Comprehensive Physiology

433

388

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“…TRH or TRH analogs injected into the cisterna magna increase efferent activity in the gastric branch of the vagus nerve (8a) and increases vagal muscarinic-dependent stimulation of gastric acid, pepsin, histamine, and serotonin secretion, mucosal blood flow (MBF), emptying, and contractility (2,12,13,15,23,24). Gastric acid secretion peaks within 20 -30 min after TRH injection and returns to the preinjection level in 90 -120 min (13,20).…”

Section: Discussionmentioning

confidence: 99%

“…Sustained increases in acid secretion induced by RX-77368 are important for ulcerogenic effects of the peptide. Although pepsin or histamine secretion, mast cell, or contractility may be related to the initial increase in RX-77368-induced gastric mucosal permeability (2,9,23,24), the specific factors that are related to the initial increase in permeability remain to be investigated in detail.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of early gastric mucosal permeability induced by central thyrotropin-releasing hormone administration

Joh¹

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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2004.-Accumulating evidence suggests that central thyrotropin-releasing hormone (TRH) administration induces gastric erosion 4 h after administration through the vagal nerves. However, early changes in the gastric mucosa during these 4 h have not been described. To assess early changes in the gastric mucosa after intracisternal injection of a stable TRH analog, pGlu-His-(3,3Ј-dimethyl)-ProNH 2 (RX-77368), we measured the blood-to-lumen 51 Cr-labeled EDTA clearance and examined the effects of vagotomy, atropine, omeprazole, and hydrochloric acid (HCl) on RX-77368-induced mucosal permeability. A cytoprotective dose of RX-77368 (1.5 ng) did not increase mucosal permeability. However, higher doses significantly increased mucosal permeability. Permeability peaked within 20 min and gradually returned to control levels in response to a 15-ng dose (submaximal dose). Increased mucosal permeability was not recovered after a 150-ng dose (ulcerogenic dose). This increase in permeability was inhibited by vagotomy or atropine. Intragastric perfusion with HCl did not change the RX-77368 (15 ng)-induced increase in permeability, but completely inhibited the recovery of permeability after the peak. Pretreatment with omeprazole did not change the RX-77368 (15 ng)-induced increase in permeability, but quickened the recovery of permeability after the peak. These data indicate that the RX-77368-induced increase in permeability is mediated via the vagal-cholinergic pathway and is not a secondary change in RX-77368-induced acid secretion. Inhibited recovery of permeability on exposure to an ulcerogenic RX-77368 dose or on exposure to HCl plus a submaximal dose of RX-77368 may be crucial for the induction of gastric mucosal lesions by central RX-77368 administration. intracisternal injection; 51 Cr-labeled EDTA clearance THE ROLE OF THE CENTRAL NERVOUS SYSTEM in the regulation of gastric function has long been recognized. Thyrotropin-releasing hormone (TRH), a stress-related neuropeptide originally isolated from the hypothalamus (1, 10), or its stable analog pGlu-His-(3,3Ј-dimethyl)-ProNH 2 (RX-77368) has been reported to act in the brain to stimulate gastrointestinal secretion, motility, transit, and ulcer formation in conscious or anesthetized rats, rabbits, and cats (14, 15). Many studies (14,15) indicate that TRH actions on gut function are mediated through activation of the parasympathetic outflow and peripheral muscarinic receptors. TRH or stable TRH analogs injected into the cisterna magna show cytoprotective (19, 25) and ulcerogenic effects (3, 14) on gastric mucosa (17, 18). These stress-related effects on gastric mucosa depend on the balance between vagally activated increases in ulcerogenic agents including acid secretion (16) and cytoprotective factors such as prostaglandins (25) and heat shock proteins (8).Mucosal permeability plays a key role in regulation of gastric integrity. Although the vagal cholinergic-mediated effects of gastric acid secretion or mucosal blood flow on gut function are well characterized in response...

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“…Many of the same effects can be produced by electrically stimulating, or by the injection of RX 77368 near the nerve cell bodies in the raphe nuclei whose axons terminate in the DMV (84,(124)(125)(126). Many of the same effects can be produced by electrically stimulating, or by the injection of RX 77368 near the nerve cell bodies in the raphe nuclei whose axons terminate in the DMV (84,(124)(125)(126).…”

Section: Trh Stimulates Acid Secretion From Additional Brain Sitesmentioning

confidence: 99%

From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

Weiner

1991

Psychosomatic Medicine

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Considerable progress has been made in the understanding of the formation of gastric erosions in rats. The role of gastric acid secretion in their pathogenesis has been clarified. Gastric erosions are also associated with slow gastric contractions. With several experimental procedures, the body temperature falls; preventing this decrease averts erosions. A fall in body temperature or exposure to cold is associated with the secretion of thyrotropin-releasing hormone (TRH), and both an increase and decrease in corticotropin-releasing factor (CRF) in discrete regions of rat brains. TRH produces gastric erosions, increases in acid secretion, and slow contractions, while CRF has the opposite effects. One of the major sites of interaction of the two peptides is in the dorsal motor complex of the vagus nerve. TRH increases serotonin (5-HT) secretion into the stomach. 5-HT counter-regulates acid secretion and slow contractions. Many other peptides stimulate or inhibit gastric acid secretion.

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Excitation of neurons in the medullary raphe increases gastric acid and pepsin production in cats

Cited by 13 publications

References 0 publications

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Evaluation of early gastric mucosal permeability induced by central thyrotropin-releasing hormone administration

From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

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