Neuroendocrinology of gastric H+ and duodenal HCO3− secretion: the role of brain–gut axis

Konturek, Peter C.; Konturek, Stanisław J.; Ochmański, W

doi:10.1016/j.ejphar.2004.06.060

Cited by 15 publications

(4 citation statements)

References 52 publications

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“…The influence of the CNS over gastric secretion was famously first described by William Beaumont in 1833 [reprinted with editorial comments by Combe (40)] who noted that the acid secretion was affected by “fear, anger, and whatever depresses or disturbs the nervous system.” The role of the vagus nerve in gastric secretion was later confirmed by Pavlov in 1902 who noted that the cephalic phase of acid secretion is mediated entirely by the vagus nerve. In contrast, the gastric and intestinal phases of acid secretion involve the activation of both vagal and spinal reflexes in response to GI distention and/or the activation of mucosal receptors [reviewed in (270)]. Neurophysiological studies, notably electrical stimulation or lesion of discrete central nuclei, have highlighted the role of several areas within the brain in the control of gastric acid secretion, particularly the hypothalamus (lateral, ventromedial, and paraventricular nuclei), the locus coeruleus (LC), the caudal medullary raphe nuclei and the amygdala, as discussed in more detail below.…”

Section: Vagal Efferent Motoneuronsmentioning

confidence: 99%

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

Browning

Travagli

2014

Comprehensive Physiology

431

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%

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

Browning

Travagli

2014

Comprehensive Physiology

431

388

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“…Because activation of vagal efferent fibers can induce both excitatory as well as inhibitory effects on gastric smooth muscles (18,38,62,66,, it is clear that both excitatory and inhibitory postganglionic neuroeffectors are released from enteric neurons in response to excitatory vagal input. Note that the inhibitory vagal action on the stomach is directed toward the control of motility and tone but not of gastric secretion (181)(182)(183)(184)(185).…”

Section: Vagal Efferent (Motor) Controlmentioning

confidence: 99%

Brainstem Circuits Regulating Gastric Function

Travagli

Hermann

Browning

et al. 2006

Annu. Rev. Physiol.

437

430

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Brainstem parasympathetic circuits that modulate digestive functions of the stomach are comprised of afferent vagal fibers, neurons of the nucleus tractus solitarius (NTS), and the efferent fibers originating in the dorsal motor nucleus of the vagus (DMV). A large body of evidence has shown that neuronal communications between the NTS and the DMV are plastic and are regulated by the presence of a variety of neurotransmitters and circulating hormones as well as the presence, or absence, of afferent input to the NTS. These data suggest that descending central nervous system inputs as well as hormonal and afferent feedback resulting from the digestive process can powerfully regulate vago-vagal reflex sensitivity. This paper first reviews the essential "static" organization and function of vago-vagal gastric control neurocircuitry. We then present data on the opioidergic modulation of NTS connections with the DMV as an example of the "gating" of these reflexes, i.e., how neurotransmitters, hormones, and vagal afferent traffic can make an otherwise static autonomic reflex highly plastic.

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“…The signaling pathways triggered by H + that lead to HCO 3 ‐ secretion are unclear, although early experiments suggested the involvement of humoral factors, such as prostaglandins (10–12). In addition, experiments using dog (13), pig (14), or rat (15, 16) intestine suggested that NO and, based on the stomach physiology, some neuronal circuits may be involved in the signaling pathways (10, 17, 18). No direct downstream targets were identified in these experiments.…”

mentioning

confidence: 99%

Neuronal cGMP kinase I is essential for stimulation of duodenal bicarbonate secretion by luminal acid

et al. 2012

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Brief contact of the duodenal mucosa with luminal acid elicits a long-lasting bicarbonate (HCO(3)(-)) secretory response, which is believed to be the primary protective mechanism against mucosal damage. Here, we show that cGMP-dependent protein kinase type I-knockout (cGKI(-/-)) mice are unable to respond to a physiological H(+) stimulus with a HCO(3)(-) secretory response and spontaneously develop duodenal ulcerations. Smooth muscle-selective cGKI knock-in rescued the motility disturbance but not the defective HCO(3)(-) secretion. Proton-induced HCO(3)(-) secretion was not attenuated by selective inactivation of the cGKI gene in interstitial cells of Cajal or in enterocytes, but was abolished by inactivation of cGKI in neurons (ncGKI(-/-)). cGKI was expressed in the brainstem nucleus tractus solitarius that connects the afferent with the efferent N. vagus. Accordingly, truncation of the subdiaphragmal N. vagus significantly diminished proton-induced HCO(3)(-) secretion in wild-type mice, whereas stimulation of the subdiaphragmal N. vagus elicited a similar HCO(3)(-) secretory response in cGKI(-/-), ncGKI(-/-) and wild-type mice. These findings show that protection of the duodenum from acid injury requires neuronal cGKI.

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Neuroendocrinology of gastric H+ and duodenal HCO3− secretion: the role of brain–gut axis

Cited by 15 publications

References 52 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

Brainstem Circuits Regulating Gastric Function

Neuronal cGMP kinase I is essential for stimulation of duodenal bicarbonate secretion by luminal acid

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