Visceral pain is a global term used to describe pain originating from the internal organs of the body, which affects a significant proportion of the population and is a common feature of functional gastrointestinal disorders (FGIDs) such as irritable bowel syndrome (IBS). While IBS is multifactorial, with no single etiology to completely explain the disorder, many patients also experience comorbid behavioral disorders, such as anxiety or depression; thus, IBS is described as a disorder of the gut-brain axis. Stress is implicated in the development and exacerbation of visceral pain disorders. Chronic stress can modify central pain circuitry, as well as change motility and permeability throughout the gastrointestinal (GI) tract. More recently, the role of the gut microbiota in the bidirectional communication along the gut-brain axis, and subsequent changes in behavior, has emerged. Thus, stress and the gut microbiota can interact through complementary or opposing factors to influence visceral nociceptive behaviors. This review will highlight the evidence by which stress and the gut microbiota interact in the regulation of visceral nociception. We will focus on the influence of stress on the microbiota and the mechanisms by which microbiota can affect the stress response and behavioral outcomes with an emphasis on visceral pain.

/pdf/stress-and-the-microbiota-gut-brain-axis-in-visceral-pain-194bfttc2n.pdf

Stress and the Microbiota-Gut-Brain Axis in Visceral Pain: Relevance to Irritable Bowel Syndrome.

Anxiety disorders are the most common mental illness in the USA affecting 18% of the population. The cause(s) of anxiety disorders is/are not completely clear, and research in the neurobiology of anxiety at the molecular level is still rather limited. Although mounting clinical and preclinical evidence now indicates that oxidative stress may be a major component of anxiety pathology, whether oxidative stress is the cause or consequence remains elusive. Studies conducted over the past few years suggest that anxiety disorders may be characterised by lowered antioxidant defences and increased oxidative damage to proteins, lipids, and nucleic acids. In particular, oxidative modifications to proteins have actually been proposed as a potential factor in the onset and progression of several psychiatric disorders, including anxiety and depressive disorders. Oxidised proteins are normally degraded by the proteasome proteolytic complex in the cell cytoplasm, nucleus, and endoplasmic reticulum. The Lon protease performs a similar protective function inside mitochondria. Impairment of the proteasome and/or the Lon protease results in the accumulation of toxic oxidised proteins in the brain, which can cause severe neuronal trauma. Recent evidence points to possible proteolytic dysfunction and accumulation of damaged, oxidised proteins as factors that may determine the appearance and severity of psychotic symptoms in mood disorders. Thus, critical interactions between oxidative stress, proteasome, and the Lon protease may provide keys to the molecular mechanisms involved in emotional regulation, and may also be of great help in designing and screening novel anxiolytics and antidepressants.

The role of oxidative stress in anxiety disorder: cause or consequence?

IntroductionInflammatory bowel disease (IBD) is a chronic relapsing and remitting disorder characterised by inflammation of the gastrointestinal tract. There is a growing consensus that IBD is associated with anxiety- and depression-related symptoms. Psychological symptoms appear to be more prevalent during active disease states with no difference in prevalence between Crohn’s disease and ulcerative colitis. Behavioural disturbances including anxiety- and depression-like symptoms have also been observed in animal models of IBD.ResultsThe likely mechanisms underlying the association are discussed with particular reference to communication between the gut and brain. The close bidirectional relationship known as the gut–brain axis includes neural, hormonal and immune communication links. Evidence is provided for a number of interacting factors including activation of the inflammatory response system in the brain, the hypothalamic–pituitary–adrenal axis, and brain areas implicated in altered behaviours, changes in blood brain barrier integrity, and an emerging role for gut microbiota and response to probiotics in IBD.DiscussionThe impact of psychological stress in models of IBD remains somewhat conflicted, however, it is weighted in favour of stress or early stressful life events as risk factors in the development of IBD, stress-induced exacerbation of inflammation and relapse.ConclusionIt is recommended that patients with IBD be screened for psychological disturbance and treated accordingly as intervention can improve quality of life and may reduce relapse rates.

/pdf/gut-brain-actions-underlying-comorbid-anxiety-and-depression-3chjkd6jca.pdf

Gut-brain actions underlying comorbid anxiety and depression associated with inflammatory bowel disease.

Inflammatory bowel disease (IBD) causes severe physical symptoms and is also associated with psychological comorbidities. Abnormal anxiety levels are found in up to 40% of patients with IBD. Anxiety symptoms are often related to flares of IBD but may persist in times of remission. Detection of anxiety disorder (AD) in patients with IBD can be challenging. Patients with anxiety may also exhibit symptoms in keeping with functional gastrointestinal disorders (FGID). Evidence for the effectiveness of pharmacological and psychological therapies for anxiety stems from patients without IBD. Studies in patients with IBD have either been small or shown negative results. In light of this, a combined approach involving IBD physicians to improve disease control and psychologists or psychiatrists to treat anxiety is advised. This review examines the evidence of anxiety issues in IBD with a focus on extent of the problem, risk factors for anxiety, and the effectiveness of interventions.

/pdf/inflammatory-bowel-disease-and-anxiety-links-risks-and-5rt5031m7m.pdf

Inflammatory bowel disease and anxiety: links, risks, and challenges faced.

Voltage-gated sodium channels (NaV channels) are essential for the initiation and propagation of action potentials that critically influence our ability to respond to a diverse range of stimuli. Physiological and pharmacological studies have linked abnormal function of NaV channels to many human disorders, including chronic neuropathic pain. These findings, along with the description of the functional properties and expression pattern of NaV channel subtypes, are helping to uncover subtype specific roles in acute and chronic pain and revealing potential opportunities to target these with selective inhibitors. High-throughput screens and automated electrophysiology platforms have identified natural toxins as a promising group of molecules for the development of target-specific analgesics. In this review, the role of toxins in defining the contribution of NaV channels in acute and chronic pain states and their potential to be used as analgesic therapies are discussed.

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/bph.13962

Sodium channels and pain: from toxins to therapies.

Background Previous studies found that visceral sensitivity is increased in bowel obstruction (BO). We hypothesized that mechanical stress-induced expression of BDNF in smooth muscle cells (SMC) of the distended bowel plays a critical role in visceral hypersensitivity in BO by altering voltage-gated K+ channel (Kv ) activity in sensory neurons. Methods Partial colon obstruction was maintained in rats for 7 days. Colon-projecting neurons in the dorsal root ganglia (DRG, T13 to L2) were isolated for electrophysiological and gene expression studies. Key results Compared to controls, membrane excitability of colon-projecting DRG neurons was markedly enhanced in BO. The densities of total Kv and transient A-type (IA ) K+ currents, but not sustained delayed IK current, were significantly reduced in the neurons in BO. The mRNA expression of IA subtype Kv 1.4 in colon neurons was down-regulated in BO. Expression of BDNF mRNA and protein was dramatically increased in colonic smooth muscle of the distended segment, but not in the non-distended aboral segment. Mechanical stretch of colon SMC in vitro increased BDNF expression. Treatment with anti-BDNF antibody restored total Kv and IA currents of neurons from BO rats. Administration of Trk B inhibitor ANA-12 blocked BO-associated changes of neuronal excitability, Kv activity and gene expression in obstruction. Conclusions and inferences Mechanical stress-induced expression of BDNF in colon SMC plays a critical role in visceral hypersensitivity in BO by suppressing A-type K+ currents and gene expression in sensory nerve. These findings help to identify therapeutic targets for distention-associated abdominal pain in the gut.

/pdf/role-of-brain-derived-neurotrophic-factor-in-the-4bbk37dfp7.pdf

Role of brain-derived neurotrophic factor in the pathogenesis of distention-associated abdominal pain in bowel obstruction.

Our preclinical study shows that fecal retention is a pathogenic factor in opioid-induced bowel dysfunction, as prevention of fecal retention with liquid diet improved motility and attenuated visce...

An opioid receptor-independent mechanism underlies motility dysfunction and visceral hyperalgesia in opioid-induced bowel dysfunction.

Stretch-Induced BDNF in Colon Smooth Muscle Plays a Critical Role in Obstruction Associated Visceral Hypersensitivity by Altering K v Function in Primary Sensory Neurons

Mo1857 Suppressed A-type K+ Current Accounts for Enhanced Excitability of Colon Specific Sensory Neurons in a Rat Model of Irritable Bowel Syndrome: Therapeutic Improvements by Electroacupuncture

255 Mechanotranscription Plays a Critical Role in Smooth Muscle Hyperplasia in Bowel Obstruction

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