Neuropathophysiology of functional gastrointestinal disorders

Wood, Jackie D.

doi:10.3748/wjg.v13.i9.1313

Cited by 100 publications

(81 citation statements)

References 171 publications

(224 reference statements)

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“…Reviews describing changes in expression of cotransmitters and receptors in diseased gut are available (40,89,90). VIP levels are reduced in the myenteric plexus and muscle layers of patients with idiopathic constipation, whereas levels of 5-HT are increased, and SP and NPY are normal.…”

Section: Pathophysiology Of Autonomic Neurotransmissionmentioning

confidence: 99%

Autonomic Neurotransmission: 60 Years Since Sir Henry Dale

Burnstock

2009

Annu. Rev. Pharmacol. Toxicol.

109

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In the early twentieth century, Sir Henry Dale and others described brilliant studies of autonomic neurotransmission utilizing acetylcholine and noradrenaline. However, within the past 60 years, new discoveries have changed our understanding of the organization of the autonomic nervous system, including the structure and function of the nonsynaptic autonomic neuroeffector junction, the multiplicity of neurotransmitters, cotransmission, neuromodulation, dual control of vascular tone by perivascular nerves and endothelial cells, the molecular biology of receptors, and trophic signaling. Further, it is now recognized that an outstanding feature of autonomic neurotransmission is the inherent plasticity afforded by its structural and neurochemical organization and the interaction between expression of neural mediators and environmental factors. In this way, autonomic neurotransmission is matched to ongoing changes in demands and can sometimes be compensatory in pathophysiological situations.

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Section: Pathophysiology Of Autonomic Neurotransmissionmentioning

confidence: 99%

Autonomic Neurotransmission: 60 Years Since Sir Henry Dale

Burnstock

2009

Annu. Rev. Pharmacol. Toxicol.

109

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“…These functions are relevant for the control of inflammation, absorption and secretion, transport of macromolecules, and metabolic processes. 11 Moreover, most of the cellular components have been shown to express receptors for CRF. 12,13 But the job of the intestinal barrier now appears to be far more nuanced and complex as it communicates multidirectionally with the immune system and the microbes.…”

Section: Intestinal Permeabilitymentioning

confidence: 99%

Role of Corticotropin-releasing Factor in Gastrointestinal Permeability

Rodiño-Janeiro¹,

Alonso-Cotoner²,

Pigrau³

et al. 2015

J Neurogastroenterol Motil

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The interface between the intestinal lumen and the mucosa is the location where the majority of ingested immunogenic particles face the scrutiny of the vast gastrointestinal immune system. Upon regular physiological conditions, the intestinal microflora and the epithelial barrier are well prepared to process daily a huge amount of food-derived antigens and non-immunogenic particles. Similarly, they are ready to prevent environmental toxins and microbial antigens to penetrate further and interact with the mucosal-associated immune system. These functions promote the development of proper immune responses and oral tolerance and prevent disease and inflammation. Brain-gut axis structures participate in the processing and execution of response signals to external and internal stimuli. The brain-gut axis integrates local and distant regulatory networks and supersystems that serve key housekeeping physiological functions including the balanced functioning of the intestinal barrier. Disturbance of the brain-gut axis may induce intestinal barrier dysfunction, increasing the risk of uncontrolled immunological reactions, which may indeed trigger transient mucosal inflammation and gut disease. There is a large body of evidence indicating that stress, through the brain-gut axis, may cause intestinal barrier dysfunction, mainly via the systemic and peripheral release of corticotropin-releasing factor. In this review, we describe the role of stress and corticotropin-releasing factor in the regulation of gastrointestinal permeability, and discuss the link to both health and pathological conditions. (J Neurogastroenterol Motil 2015;21:33-50)

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“…Gastric motility is regulated through enteric nervous system activity and involves both excitatory cholinergic and inhibitory nitrergic neurons (36). NO is the nonadrenergic, noncholinergic (NANC) neurotransmitter released from nitrergic neurons, resulting in sphincter muscle relaxation (6).…”

mentioning

confidence: 99%

Tetrahydrobiopterin deficiency induces gastroparesis in newborn mice

Welsh

Enomoto

Pan

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Pyloric stenosis, the most common infant gastrointestinal disease, has no known etiology and clinically presents as abnormal gastric emptying with evidence of pyloric muscle hypertrophy. Whether abnormalities in gastric muscle contraction and/or relaxation have a role in this condition is poorly known, but gastroparesis is commonly observed in association with delayed gastric emptying in adults. Therefore, we evaluated the tetrahydrobiopterin (BH4)-deficient newborn mouse model of this disease (hph-1) and hypothesized that their gastric muscle properties are impaired, when compared with wild-type control animals. In vitro studies evaluating the age-dependent gastric fundus muscle contraction and relaxation potential were conducted. Compared with wild-type mice, the hph-1 stomach content/body weight ratio was significantly increased in newborn but not juvenile or adult animals, confirming abnormal gastric emptying. Gastric tissue neuronal nitric oxide synthase (nNOS) protein expression was upregulated in both newborn and adult hph-1 mice, but in the former there was evidence of enzyme uncoupling and higher tissue superoxide generation when compared with same age-matched animals. As opposed to the lack of strain differences in the U46619-induced force, the newborn hph-1 gastric muscle carbachol-induced contraction and nNOS-dependent relaxation were significantly reduced (P Ͻ 0.01). These group differences were not present in juvenile or adult mice. Preincubation with BH4 significantly enhanced the newborn hph-1, but not wild-type, gastric muscle contraction. In conclusion, changes compatible with gastroparesis are present in the newborn mouse model of pyloric stenosis. The role of BH4 deficiency and possibly associated gastroparesis in the pathogenesis of infantile pyloric stenosis warrants further investigation. pylorus; gastric emptying; nitric oxide INFANTILE HYPERTROPHIC PYLORIC stenosis (IHPS) is a relatively common condition of unknown etiology and pathogenesis. Infants with this condition seldom exhibit any abnormalities at birth. The gastric outlet obstruction develops at 2-12 wk of life, and the pyloric sphincter hypertrophy quickly resolves after pyloromyotomy, a surgical intervention involving the longitudinal incision of the circular muscle (23,27,28).IHPS has traditionally been seen as a condition resulting from failure of the pyloric sphincter muscle to relax, thus preventing adequate and rapid gastric emptying following a meal. Infants with IHPS have a lower plasma nitrate level when compared with age-matched controls, and, following pyloromyotomy, the nitrate concentration increases to values found in normal infants (17). The pyloric tissue neuronal nitric oxide synthase (nNOS) expression is reduced in subjects with IHPS (1). Given nNOS role in NO generation, this has been postulated to play a significant role in the muscle hypertrophy and reduced sphincter relaxation observed in this condition.Gastric motility is regulated through enteric nervous system activity and involves both excitatory cholin...

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Neuropathophysiology of functional gastrointestinal disorders

Cited by 100 publications

References 171 publications

Autonomic Neurotransmission: 60 Years Since Sir Henry Dale

Autonomic Neurotransmission: 60 Years Since Sir Henry Dale

Role of Corticotropin-releasing Factor in Gastrointestinal Permeability

Tetrahydrobiopterin deficiency induces gastroparesis in newborn mice

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