Mechanical activation of vagal afferents involves opposing cation and TREK1 currents and NO regulation.

Vagal afferents convey signals of mechanical stimulation in the gut to the brain, which is essential for the regulation of food intake. However, ion channels sensing mechanical stimuli are not fully understood. This study aimed to examine the ionic currents activated by mechanical stimulation and a possible neuro-modulatory role of nitric oxide on vagal afferents.

Mechanisms of reduced leptin-mediated satiety signaling during obesity.

Background/objectives: Disrupted leptin signaling in vagal afferent neurons contributes to hyperphagia and obesity. Thus, we tested the hypothesis that intrinsic negative regulators of leptin signaling, suppressor of cytokine signaling 3 (SOCS3) and protein tyrosine phosphatase 1B (PTP1B) underlie dysfunctional leptin-mediated vagal afferent satiety signaling during obesity.

Methods: Experiments were performed on standard chow-fed control mice, high-fat fed (HFF), or low-fat fed (LFF) mice.

Are psychological interventions effective in treating functional dyspepsia? A systematic review and meta-analysis.

Background And Aim: Functional dyspepsia (FD) is a common gastrointestinal disorder, characterized primarily by postprandial fullness or early satiety and/or pain in the epigastrium with no endoscopic evidence of disease. Psychological therapies have been adapted to the treatment of disordered gut-brain interaction such as FD. We sought to determine if psychological interventions were efficacious in providing symptom management and improving health-related quality of life in patients suffering from FD.

Effect of high-fat diet on mechanosensitive transient receptor potential channel activation in vagal afferent neurons.

Mechanical stimulation of the gastrointestinal tract is an important stimulus of satiety and can be transduced by transient receptor potential (TRP) channels. Several studies have revealed attenuated vagally-mediated satiety responses including mechanosensitivity in diet-induced obesity; however, ion channels underlying this hyposensitivity have not been fully understood. This study aimed to examine the effect of chronic high-fat diet on activation of selected mechanosensitive TRP channels in vagal afferents.

Chronic high fat diet impairs glucagon like peptide-1 sensitivity in vagal afferents.

Dysfunction of the gut-brain axis is one of the potential contributors to the pathophysiology of obesity and is therefore a potential target for treatment. Vagal afferents innervating the gut play an important role in controlling energy homeostasis. There is an increasing evidence for the role of vagal afferents in mediating the anorexigenic effects of glucagon-like peptide-1 (GLP-1), an important satiety and incretin hormone.

Examining Psychosocial Mechanisms of Pain-Related Disability in Inflammatory Bowel Disease.

Disability in inflammatory bowel disease (IBD) is under-investigated. Models theorize that disability is the result of a disease and its related impairments, limitations, and restrictions. This disablement process can be affected by psychosocial factors.

Inducible nitric oxide synthase-derived nitric oxide reduces vagal satiety signalling in obese mice.

Key Points: Obesity is associated with disrupted satiety regulation. Mice with diet-induced obesity have reduced vagal afferent neuronal excitability and a decreased afferent response to satiety signals. A low grade inflammation occurs in obesity with increased expression of inducible nitric oxide synthase (iNOS).

Increased TASK channel-mediated currents underlie high-fat diet induced vagal afferent dysfunction.

We have previously demonstrated that satiety sensing vagal afferent neurons are less responsive to meal-related stimuli in obesity because of reduced electrical excitability. As leak K currents are key determinants of membrane excitability, we hypothesized that leak K currents are increased in vagal afferents during obesity. Diet-induced obesity was induced by feeding C57Bl/6J mice a high-fat diet (HFF) (60% energy from fat) for 8-10 wk.

Anti-Hu antibodies activate enteric and sensory neurons.

IgG of type 1 anti-neuronal nuclear antibody (ANNA-1, anti-Hu) specificity is a serological marker of paraneoplastic neurological autoimmunity (including enteric/autonomic) usually related to small-cell lung carcinoma. We show here that IgG isolated from such sera and also affinity-purified anti-HuD label enteric neurons and cause an immediate spike discharge in enteric and visceral sensory neurons. Both labelling and activation of enteric neurons was prevented by preincubation with the HuD antigen.

Mechanisms of Quality of Life and Social Support in Inflammatory Bowel Disease.

Cognitive and social factors are essential considerations in inflammatory bowel disease (IBD) patient management, but existing research is limited. This study aims to expand the IBD literature by examining the relationship between social supports and QoL, while examining mechanisms in these relationships. Consenting patients attending an IBD outpatient clinic were provided a survey package (N = 164).

Effects of inflammation on the innervation of the colon.

Inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease lead to altered gastrointestinal (GI) function as a consequence of the effects of inflammation on the tissues that comprise the GI tract. Among these tissues are several types of neurons that detect the state of the GI tract, transmit pain, and regulate functions such as motility, secretion, and blood flow. This review article describes the structure and function of the enteric nervous system, which is embedded within the gut wall, the sympathetic motor innervation of the colon and the extrinsic afferent innervation of the colon, and considers the evidence that colitis alters these important sensory and motor systems.

The long chain fatty acid oleate activates mouse intestinal afferent nerves in vitro.

Vagal afferents innervating the gastrointestinal tract serve an important nutrient-sensing function, and these signals contribute to satiety. Detection of nutrients occurs largely through the release of mediators from specialized enteroendocrine cells within the mucosa of the gastrointestinal tract. The signaling pathways leading to vagal afferent activation are not clear; however, previous in-vivo studies have implicated a role for cholecystokinin (CCK).

Impaired intestinal afferent nerve satiety signalling and vagal afferent excitability in diet induced obesity in the mouse.

Gastrointestinal vagal afferents transmit satiety signals to the brain via both chemical and mechanical mechanisms. There is indirect evidence that these signals may be attenuated in obesity. We hypothesized that responses to satiety mediators and distension of the gut would be attenuated after induction of diet induced obesity.

Visceral afferents - determinants and modulation of excitability.

An essential property of visceral sensory afferents is to be able to alter their firing properties in response to changes in the microenvironment at the level of the sensory ending. Significant progress has been made in recent years in understanding the ionic mechanisms of the regulation of afferent neuronal excitability, and in identifying the mechanisms by which this can be altered. This article will review some of the recent developments in the state of knowledge regarding mechanisms of increased excitability after inflammation, and pharmacological modulation of excitability, concentrating on afferent nerves innervating the GI tract and urinary bladder.

Two TTX-resistant Na+ currents in mouse colonic dorsal root ganglia neurons and their role in colitis-induced hyperexcitability.

The composition of Na+ currents in dorsal root ganglia (DRG) neurons depends on their neuronal phenotype and innervation target. Two TTX-resistant (TTX-R) Na+ currents [voltage-gated Na channels (Nav)] have been described in small DRG neurons; one with slow inactivation kinetics (Nav1.8) and the other with persistent kinetics (Nav1.

Ileitis modulates potassium and sodium currents in guinea pig dorsal root ganglia sensory neurons.

Intestinal inflammation induces hyperexcitability of dorsal root ganglia sensory neurons, which has been implicated in increased pain sensation. This study examined whether alteration of sodium (Na+) and/or potassium (K+) currents underlies this hyperexcitability. Ileitis was induced in guinea pig ileum with trinitrobenzene sulphonic acid (TBNS) and dorsal root ganglion neurons innervating the site of inflammation were identified by Fast Blue or DiI fluorescence labelling.