In contrast to the CeA, however, lesions of the BNST exacerbate gastric lesions induced by stressors (213, 343). The microbiome-gut-brain axis: From bowel to behavior. Kalia M, Fuxe K, Goldstein M, Harfstrand A, Agnati LF, Coyle JT. Furthermore, electrical stimulation of the PVN induces a vagally dependent decrease in gastric motility and increase in gastric acid secretion (404), actions that are blocked by DVC application of an OXY antagonist and mimicked by microinjection of an OXY agonist. Stimulation The stimulation for these contractions likely originates in modified smooth muscle cells called interstitial cells of Cajal. Medullary raphe: A new site for vagally mediated stimulated of gastric motility in cats. Vagal afferents that transduce and relay information from the GI tract can be classified based upon their response to distention or pressure (principally low-threshold, although nociceptive high-threshold fibers also exist), the location of their receptive fields (mucosal, muscle, or serosal/mesenteric), their preferred stimulus modality (chemical, osmotic, mechanical, both in-series and in-parallel) or the region of GI tract innervated [reviewed in (52)]. Andresen MC, Kunze DL. Furuse M, Matsumoto M, Mori R, Sugahara K, Kano K, Hasegawa S. Influence of fasting and neuropeptide Y on the suppressive food intake induced by intracerebroventricular injection of glucagon-like peptide-1 in the neonatal chick. De Groat WC, Nadelhaft I, Milne RJ, Booth AM, Morgan C, Thor K. Organization of the sacral parasympathetic reflex pathways to the urinary bladder and large intestine. Vagally mediated effects of glucagon-like peptide 1: In vitro and in vivo gastric actions. The response of vagal motoneurons to neurotransmitters or neuromodulators does not appear to be static, however. Vizzard MA, Brisson M, De Groat WC. Miller MA, Vician L, Clifton DK, Dorsa DM. Selective enhancement of synaptic inhibition by hypocretin (orexin) in rat vagal motor neurons: Implications for autonomic regulation. Long-term expression of corticotropin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus in response to an acute colonic inflammation. AParea postrema; DMVdorsal motor nucleus of the vagus; NTSnucleus of the tractus solitarius; PB Complexparabrachial complex (i.e., parabrachial nucleus + Klliker-Fuse nucleus); PAGperiaqueductal gray; CeAcentral nucleus of the amygdala; Vestibular Nvestibular nucleus; Trigeminal Ntrigeminal nucleus; Raphe Nraphe nuclei. Intestinal glucose-induced calcium-calmodulin kinase signaling in the gutbrain axis in awake rats. Role of the cerebellum in the control of gastro-intestinal motility. Tache Y, Bonaz B. Corticotropin-releasing factor receptors and stress-related alterations of gut motor function. Chronwall BM. The LC (A6 noradrenergic region), located within the rostral pons at the lateral floor of the fourth ventricle, is the brains predominant source of noradrenergic innervation. Projections from the parabrachial nucleus to the vestibular nuclei: Potential substrates for autonomic and limbic influences on vestibular responses. Altschuler SM, Escardo J, Lynn RB, Miselis RR. Tran L, Greenwood-Van Meerveld B. Altered expression of glucocorticoid receptor and corticotropin-releasing factor in the central amygdala in response to elevated corticosterone. The standardization of experimental techniques between groups of researchers would also be advantageous in comparing experimental outcomes; note, for example, the differential effects of anesthetics on gastric emptying rates (384). Gulbransen BD, Sharkey KA. (109) found that the LC does not innervate the dorsal commissural nucleus of the thoracic spinal cord and was, therefore, unlikely to influence the activity of sympathetic preganglionic neurons innervating the upper GI tract. Indeed, studies have demonstrated that PB complex neurons may receive converging inputs from vestibular and visceral vagal afferents (453) and from orosensory and visceral vagal afferents (259) suggesting some potential for integration of afferent information. Fisk GD, Wyss JM. Glaum SR, Miller RJ. 1). Balaban CD. A nitric oxide and prostaglandin-dependent component of NANC off-contractions in cat colon. Patients with FD exhibit gastric dysmotility following stress; anger, for example, inhibits gastric motility in FD patients but not in healthy volunteers. Roosen L, Boesmans W, Dondeyne M, Depoortere I, Tack J, Vanden Berghe P. Specific hunger- and satiety-induced tuning of guinea pig enteric nerve activity. Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow. Heterogeneity of metabotropic glutamate receptors in autonomic cell groups of the medulla oblongata of the rat. Ennis M, Behbehani M, Shipley MT, Van Bockstaele EJ, Aston-Jones G. Projections from the periaqueductal gray to the rostromedial pericoerulear region and nucleus locus coeruleus: Anatomic and physiologic studies. Neuronal glucosensing: What do we know after 50 years? Selective opioid agonists modulate afferent transmission in the rat nucleus tractus solitarius. Vagus nerve integrity and experimental colitis. Phillips RJ, Powley TL. Gonadal steroid hormones and the hypothalamo-pituitary-adrenal axis. Parasympathetic stimuli typically stimulate these digestive activities The enteric nervous system is located within the wall of the digestive tract, all the way from the esophagus to the . 1Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, Pennsylvania. Grammatopoulos DK. While this reflex was initially thought of as being operative in the diseased gut (i.e., activated only during malabsorbtion (449), later studies have shown that nutrients may reach the distal small intestine even under normal conditions, and re-establish the motility from the fed to the fasted pattern (264, 297). Note that the location of nuclei is not intended to be anatomically accurate. Lazovic J, Wrzos HF, Yang QX, Collins CM, Smith MB, Norgren R, Matyas K, Ouyang A. As following extrinsic denervation of the stomach, however, over time colonic motility patterns may be somewhat restored suggesting the role of parasympathetic inputs is to enhance and modulate intrinsic motility patterns rather than initiate or terminate colonic functions. The discussions above regarding the central modulation of GI functions have been written primarily from the point of normal or basal regulation. III. Tsukamoto K, Nakade Y, Mantyh C, Ludwig K, Pappas TN, Takahashi T. Peripherally administered CRF stimulates colonic motility via central CRF receptors and vagal pathways in conscious rats. Brain-gut-microbe communication in health and disease. 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 contribution of brain stem catecholamine cell groups to the innervation of the sympathetic lateral cell column. These cells are tuned to the physical properties of the surrounding tissue, so they can discriminate mechanical stimuli from the baseline mechanical state. Fos expression in serotonergic midbrain neurons projecting to the paraventricular nucleus of hypothalamus after noxious stimulation of the stomach: A triple labeling study in the rat. As with vagal sensory somata, glucose induces the trafficking of 5-HT3 receptors to the membrane of vagal sensory terminals, the tonic activation of which increases glutamate release onto NTS neurons (528). Hyperpolarization-activated currents I. Travagli RA, Gillis RA. Although GI functions are controlled by the autonomic nervous system and occur, by and large, independently of conscious perception, it is clear that the sympathetic and parasympathetic regulation and modulation of the GI tract are modulated by higher CNS centers that influence homeostatic control as well as cognitive and behavioral functions. Following stimulation of the cerebellum, gastric, and intestinal motility, as well as gastric acid secretion, are modulated by both vagally dependent as well as vagally independent pathways (298, 314). Functional magnetic resonance imaging (fMRI) and positron emission tomography techniques have demonstrated that patients exhibiting GI hypersensitivity show altered processing of visceral stimulation and increased activation of several CNS regions including the amygdala (322, 323) while rodent studies have shown an increased neuronal activation in CeA following colorectal distention (283, 533). Zhou SY, Lu YX, Owyang C. Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat. Despite the dense sympathetic innervation to the GI tract, there appears to be little tonic sympathetic activity, at least with regard to GI motility although splanchnic nerve section does result in an moderate increase in peristaltic activity (38,39). While glucose is a universal fuel for neurons, some neurons, particularly within the brainstem and hypothalamus, possess the additional ability to use variations in extracellular glucose levels to modulate their excitability (2, 148, 290). Zsombok A, Bhaskaran MD, Gao H, Derbenev AV, Smith BN. A large body of work has demonstrated that, peripherally, the activity and responsiveness of vagal sensory neurons varies according to nutritional statusthe activation of vagal reflexes will depend, therefore, on ongoing metabolic and physiological conditions. Microinjection of CRF into the LC stimulates colonic motility and accelerates colonic transit significantly but has no effect upon gastric motility or emptying (341, 462). Reduced hindbrain and enteric neuronal response to intestinal oleate in rats maintained on high-fat diet. The brain and the stress axis: The neural correlates of cortisol regulation in response to stress. Vagal afferent neurons in high fat diet-induced obesity; intestinal microflora, gut inflammation and cholecystokinin. Dopamine effects on identified rat vagal motoneurons. Damage to parasympathetic nerves, or extrinsic denervation, frequently results in dysregulated colonic motility and constipation. Choi DC, Furay AR, Evanson NK, Ostrander MM, Ulrich-Lai YM, Herman JP. Fennegan FM, Puiggari MJ. The biology of incretin hormones. While preganglionic neurons innervating the colon are, as elsewhere, cholinergic, immunohistochemical studies have identified populations of preganglionic parasympathetic enkephalinergic neurons within the S2S3 segments of the sacral spinal cord of the rat and cat (190, 262). Hypothalamic projections to locus coeruleus neurons in rat brain. Gastric hyperactivity has been observed in some rodent models of hyperglycemia and in some diabetic patients, whereas diabetic gastroparesis, defined as delayed gastric emptying accompanied by other upper GI symptoms including early satiety, nausea, fullness, bloating and abdominal pain, has been observed in others (100, 238, 435). As discussed below, stress causes the activation of CRF-containing neurons within Barringtons Nucleus and PVN that project to the LC (202, 289, 340, 342) that not only increases colonic transit but also increases arousal and anxiety-like behaviors which may be of importance in the pathophysiology of functional bowel disorders such as irritable bowel syndrome (IBS) associated with comorbid anxiety and depression (335, 461, 505). Maintenance on a high-fat diet impairs the anorexic response to glucagon-like-peptide-1 receptor activation. Browning KN, Renehan WE, Travagli RA. Browning KN, Travagli RA. Efferent projections from the LC to the cortex as well as projections to the cerebellum, thalamic relay network and amygdala provide a neuroanatomical basis for the involvement of the LC in attention and arousal [reviewed in (165)]. Krowicki ZK, Hornby PJ. Richar P, Moos F, Freund-Mercier M-J. Nutrient tasting and signaling mechanisms in the gut. Thyrotropin-releasing hormone-immunoreactive projections to the dorsal motor nucleus and the nucleus of the solitary tract of the rat. Gastric emptying of enterally administered liquid meal in conscious rats and during sustained anaesthesia. An autoradiographic study of the projections of the central nucleus of the monkey amygdala. Organization of cortical, basal forebrain, and hypothalamic afferents to the parabrachial nucleus in the rat. As in other neurons excited by elevations in glucose levels, this appears to involve the closure of an ATP-sensitive potassium channel (30, 487, 488). Spiller RC, Trotman IF, Higgins BE, Ghatei MA, Grimble GK, Lee YC, Bloom SR, Misiewicz JJ, Silk DB. The BNST projects to several areas involved in autonomic homeostatic regulation of GI functions including the NTS, DMV, PAG, hypothalamus, LC, and PB complex (46, 196, 232). Trapp S, Ballanyi K, Richter DW. NTS neurons, which provide the most prominent source of synaptic inputs to GI-projecting DMV neurons, play a critical role in shaping the activity of the efferent vagus nerve (Fig. Shepard JD, Myers DA. Cragg BG, Evans DH. Musings on the wanderer: Whats new in our understanding of vago-vagal reflexes? Direct projections from the lumbosacral spinal cord to Barringtons nucleus in the rat: A special reference to micturition reflex. Glucagon-like peptide-1 inhibits voltage-gated potassium currents in mouse nodose ganglion neurons. Opioid peptides inhibit excitatory but not inhibitory synaptic transmission in the rat dorsal motor nucleus of the vagus. Burstein R, Giesler GJ., Jr Retrograde labeling of neurons in spinal cord that project directly to nucleus accumbens or the septal nuclei in the rat. From a therapeutic standpoint, the knowledge that the CNS, via the vagus nerve, may assist in the restoration of homeostasis via the modulation of inflammatory responses provides a means by which activation of the cholinergic anti-inflammatory pathway can be exploited to treat a variety of clinical conditions. In vitro analysis of the effects of cholecystokinin on rat brain stem motoneurons. Additionally, activation of neurons within the raphe pallidus, raphe obscurus, or parapyramidal regions induces a vagally dependent increase in gastric acid secretion that is attenuated by pretreatment with DVC microinjection of a TRH antibody (176, 222). Afferents from the lower brain stem. Biochemical mapping of noradrenergic nerves arising from the rat locus coeruleus. In this regard, we have demonstrated previously that the activation of the cAMP-PKA pathway (such as following CRF exposure) modulates GABAergic synaptic transmission to gastric projecting DMV neurons for approximately 30 to 60 min before returning to prestimulation levels (73, 80). Garry RC. Nevertheless, studies in which transsynaptic virus labeling has been carried out in conjunction with selective denervation of sympathetic or parasympathetic afferents has allowed some delineation of parasympathetic versus sympathetic pathways (85,251,408; for similar studies investigating the central innervation of the pancreas). Brainstem viscerotopic organization of afferents and efferents involved in the control of swallowing. Opiate-induced molecular and cellular plasticity of ventral tegmental area and locus coeruleus catecholamine neurons. Barquist E, Bonaz B, Martinez V, Rivier J, Zinner MJ, Tache Y. Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats. Gunter WD, Shepard JD, Foreman RD, Myers DA, Greenwood-Van MB. Reichling DB, Basbaum AI. Reflex decreases in intragastric pressure in response to cholecystokinin in rats. GI dysfunction following spinal cord injury (SCI) is observed commonly in both patients and animal models at all levels of the GI tract including the esophagus (increased gastroesophageal reflux, esophagitis, and decreased esophageal contractility), stomach and upper GI tract (ulceration, dysregulated motility, altered accommodation, and delayed gastric emptying) and lower GI tract [constipation, distention; reviewed in (150,227)]. Innervation of the nucleus of the solitary tract and the dorsal vagal nucleus by thyrotropin-releasing hormone-containing raphe neurons. Distribution of dopamine receptors D1- and D2-immunoreactive neurons in the dorsal motor nucleus of vagus in rats. A significant proportion of Barringtons neurons are immunoreactive for CRF (507), indeed, CRF-immunoreactivity within this pontine region has been suggested to be a definitive marker of Barringtons nucleus (506). Certainly, pancreatic polypeptide binding sites (Y1Y5) have been identified within the DVC (312), and both NPY and PYY modulate the activity of vagal neurocircuits (33, 58, 77, 80). Gastric vagal afferents, for example, innervate neurons within the NTS gelatinosus and commisuralis while esophageal afferents innervate neurons within the NTS centralis (10, 69). An increasing body of work supports the concept that the nervous and immune systems have a complex and intricate communication network, and that crosstalk between these systems is important in the regulation of immune responses [see reviews (66, 122, 123, 321, 372, 373)]. Postganglionic sympathetic neurons innervating the stomach are contained within the celiac ganglion, while neurons innervating the intestine reside in the superior mesenteric ganglion (small intestine), the inferior mesenteric ganglion (colon) or pelvic ganglion (colon). A review. Little TJ, Horowitz M, Feinle-Bisset C. Modulation by high-fat diets of gastrointestinal function and hormones associated with the regulation of energy intake: Implications for the pathophysiology of obesity. Role of CRF in stress-related alterations of gastric and colonic motor function. Visceral cortex: A direct connection from prefrontal cortex to the solitary nucleus in rat. Valentino RJ, Miselis RR, Pavcovich LA. Vacca G, Vono P. The primary reflex effects of distension of the stomach on heart rate, arterial pressure and left ventricular contractility in the anaesthetized pig. Gray TS, Magnuson DJ. Remodeling of networks of interstitial cells of Cajal in a murine model of diabetic gastroparesis. Beglinger C, Degen L. Role of thyrotrophin releasing hormone and corticotrophin releasing factor in stress related alterations of gastrointestinal motor function. The strategic location of some portions of brainstem vagal neurocircuits outside the blood-brain barrier makes them accessible to a variety of circulating hormones, neuromodulators, and cytokines which can alter the responsiveness of vagal neurons as well as alter their ability to integrate and process the vast volume of inputs they receive from the viscera as well as other CNS areas. 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. Travagli RA, Gillis RA, Vicini S. Effects of thyrotropin-releasing hormone on neurons in rat dorsal motor nucleus of the vagus. Contribution of the locus coeruleus to the adrenergic innervation of the rat spinal cord: A biochemical study. van der Kooy D, Koda LY, McGinty JF, Gerfen CR, Bloom FE. Reflex gastric relaxation in response to distention of the duodenum. This Review provides an update on advances . Furthermore, stress-susceptible species of rodents have been found to have increased levels of CRF within the CeA (206, 439) and CeA CRF levels are also increased in animal models of colonic hypersensitivity (199, 380). 2); inputs from the NTS provide a means by which vagal sensory information can be relayed to the LC (510). The importance of vagal sensory (afferent) pathways in gut microbiota-brain communication have been demonstrated in several studies; for example, the ability of chronic probiotic treatment to alter GABA receptor expression in several CNS regions, including the cortex, amygdala, and LC, which modulate GI functions (see above) is dependent upon an intact vagus nerve (68) while vagotomy attenuates the anxiolytic actions of bifidobacteria in an animal model of colitis (44).
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