What Is The Function Of Vagus Nerve – The Vagus Nerve (VN) is the longest nerve in the body and a major component of the parasympathetic nervous system, which makes up the autonomic nervous system (ANS) with the sympathetic nervous system. There is a classical balance between the sympathetic and parasympathetic nervous systems, which is responsible for maintaining homeostasis. An imbalance of BHC is observed in various pathological conditions. The VN, a mixed nerve with 4/5 afferent and 1/5 efferent fibers, is a key component of the neuro-immune and brain-gut axis through bidirectional communication between the brain and the gastrointestinal (GI) tract. A dual anti-inflammatory role of VN has been observed using either vagal afferents targeting the hypothalamic-pituitary-adrenal axis or vagal efferents targeting the cholinergic anti-inflammatory pathway. The sympathetic nervous system and VN act in synergy, via the splenic nerve, to inhibit the release of tumor necrosis factor-alpha (TNFα) from macrophages of peripheral tissues and the spleen. Due to its anti-inflammatory effect, VN is a therapeutic target in the treatment of chronic inflammatory diseases where TNFα is a key component. In this review, we will focus on the anti-inflammatory role of VN in inflammatory bowel disease (IBD). The anti-inflammatory properties of VN can be targeted pharmacologically, with enteral nutrition, by VN stimulation (VNS), with adjunctive drugs, or by exercise. VNS is one of the alternative treatments for drug-resistant epilepsy and depression, and it is conceivable that VNS can be used as a non-drug therapy to treat inflammatory diseases of the gastrointestinal tract, such as IBD, irritable bowel syndrome, and postoperative ileus, which all are characterized by blunted autonomic balance with reduced vagal tone.
The Vagus nerve (VN), the longest nerve in the body, connects the central nervous system to the body by innervating major visceral organs such as the heart, lungs, and gastrointestinal (GI) tract. The VN is a mixed nerve with 20% efferent and 80% afferent fibers (1) and a major component of the parasympathetic nervous system, which together with the sympathetic nervous system constitutes the autonomic nervous system (ANS). The sympathetic and parasympathetic nervous systems are classically balanced to maintain homeostasis. This ANS balance is disrupted in various pathologies such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), rheumatoid arthritis (RA) and others, and such imbalance may also be a predictor of various neuro-immune diseases (2 , 3). In particular, autonomic dysfunction represented by low parasympathetic activity precedes the development of chronic inflammatory diseases such as RA (4). Therefore, autonomic dysfunction may be involved in the etiopathogenesis of inflammatory disorders rather than being a consequence of chronic inflammation. Modulation of the ANS, specifically by targeting the VN, is able to ameliorate various pathological conditions such as inflammatory disorders, including IBD, RA, obesity, and pain (5). Such modulation of VN is possible through pharmacological manipulation, VN stimulation (VNS), nutritional therapies, exercise, and adjunctive medications. VN classically does not innervate lymphoid organs; this role is dedicated to the sympathetic nervous system (6). However, the VN is involved in the neuro-immune axis through both its afferent and efferent fibers. Indeed, VN stimulates the hypothalamic-pituitary-adrenal (HPA) axis through its afferent fibers to release glucocorticoids from the adrenal glands (7). The VN also participates in the cholinergic anti-inflammatory pathway (CAP) via a vago-vagal reflex involving integrated brainstem communication between vagal afferent and efferent fibers, ie. the inflammatory reflex (8, 9). The sympathetic nervous system and VN interact through both a vago-sympathetic pathway involving vagal afferent fibers (10) and a vago-splenic pathway via vagal efferent fibers (11). Therefore, VN is at the crossroads of neuro-immune interactions, and by stimulating VN, it is possible to treat various inflammatory diseases of the body.
What Is The Function Of Vagus Nerve
In the present manuscript, first, we will describe the anatomy of the VN, second, we will characterize the interactions of the VN with the HPA axis and the CAP and the sympathetic nervous system, third, we will explore the interest of the therapeutic manipulation of the VN for anti-inflammatory properties through pharmacological activation, VNS , complementary medicines (acupuncture, hypnosis, mindfulness), enteral nutrition, exercise, and fourth, a focus on the role of VNS in modulating inflammatory disorder states and in particular the gastrointestinal tract, such as IBS, IBD and postoperative ileus (POI).
The Vagus Nerve
VN innervates the entire rat GI tract except the rectum (12). In contrast, in man, the innervation of the gastrointestinal tract by VN is debated. According to some authors, the VN innervates the digestive tract up to the splenic flexure of the colon (13) and the sacral parasympathetic nucleus innervates the rest of the intestine via the pelvic nerves; the densest innervation is provided to the stomach. However, VN can innervate the entire digestive tract in humans (14). The VN consists of 80% afferent fibers conveying gustatory, visceral, and somatic information and 20% efferent fibers involved in the control of GI motility and secretion, as well as cardiac parasympathetic tone (15) and CAP (8).
Preganglionic neurons of vagal efferents originate in the dorsal motor nucleus of the vagus (DMNV), below the nucleus tractus solitarius (NTS), where vagal afferents project. A viscerotopic distribution has been described in DMNV in rats, such that lateral neurons innervate the stomach while medial neurons innervate the colon (16). Preganglionic neurons are connected to postganglionic neurons of the enteric nervous system in the gastrointestinal tract. Acetylcholine (ACh) is the neurotransmitter released at both ends of these pre- and post-ganglionic neurons, which binds to nicotinic receptors and nicotinic or muscarinic receptors, respectively. VN is not in direct contact with the intestinal lamina propria (16), but through those enteric neurons (17), which are the effectors of VN to regulate intestinal immunity (18).
Vagus afferent fibers originate in the various intestinal layers with their cell bodies located in the nodose ganglia. They terminate in the NTS according to a rostro-caudal viscerotopic representation (19) and then to the area postrema. The DMNV forms with the NTS and area postrema the dorsal vagus complex of the brainstem, the main reflex center of the ANS. Indeed, activation of vagal afferents generates several coordinated responses (autonomic, endocrine, and behavioral) through central pathways involving the dorsal vagal complex. Viscerosensory information coming from the NTS to the DMNV influences vagal efferents at the onset of vago-vagal reflexes (20). In addition, the NTS is a relay for this peripheral information to reach multiple brain regions (21) that make up the central autonomic network (CAN) (22), such as the locus coeruleus (LC), the parabrachial (PB) nucleus, the periventricular nucleus of the thalamus, the central nucleus of the amygdala, the paraventricular nucleus of the hypothalamus (PVH), the medial preoptic area, the arcuate nucleus of the hypothalamus and the ventrolateral medulla (A1-C1 catecholaminergic nuclei) at the onset of autonomic, behavioral and endocrine response. The NTS also directly modulates the LC and its projections (23). The rostroventrolateral medulla is one of two major sources of projections to the LC (24). The latter projects to multiple cortical areas involved in stress responses but also in emotional disorders (25). The PVH projects to the bed nucleus of the stria terminalis, the dorsomedial and arcuate hypothalamic nuclei, the medial preoptic area, the periventricular nucleus of the thalamus, the PB region, and the nucleus tegmenti dorsalis lateralis (26). The PB nucleus projects back to the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and the PVH (27). The PVH projects directly to the NTS (26), thereby providing feedback to the forebrain. Therefore, visceral information (eg, nutrient sensitivity) driven by the VN is integrated into the CAN, involved in ANS functioning and HPA axis response. The VN is involved in interoceptive awareness, where the insular cortex plays a central role (28). Disruption of this interoception is seen in diseases of the digestive tract such as IBS, but also IBD. Indeed, alexithymia (29) has been observed in both (30–32).
The VN is a key component of the neuro-immune axis through both its afferent and efferent fibers. The role of vagal afferents was first described by Harris (7) in the regulation of the HPA axis. Indeed, peripheral administration of lipopolysaccharide (LPS), classically used as an experimental model of septic shock, induces the release of interleukin (IL)-1β, a proinflammatory cytokine, and finally activates vagal afferents through IL-1 receptors (33) . This effect is prevented by vagotomy (34) and is dose- and receptor-dependent (35). Vagal afferents activate NTS neurons of the A2 noradrenergic group, which project to corticotrophin-releasing factor (CRF) neurons of the parvocellular PVH. CRF then induces the release of adrenocorticotropic hormone from the pituitary gland to stimulate the release of glucocorticoids from the adrenal glands to inhibit peripheral inflammation, ie. HPA axis.
Samarpan Physiotherapy And Neuro Rehabilitation Center
In addition to this vagal afferent anti-inflammatory pathway, a second one described in 2000 by Tracey’s group involves vagal efferents (36). This group showed that stimulation of the distal end
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