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• W2158874882 abstract "EDITORIAL FOCIHindbrain contributions to anorexiaLinda RinamanLinda RinamanPublished Online:01 Nov 2004https://doi.org/10.1152/ajpregu.00437.2004MoreSectionsPDF (17 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat feeding behavior is the complex functional output of distributed neural networks, with critical components located at every level of the central neuraxis (1, 20). Nevertheless, the ability of any internal or external factor to modulate food intake ultimately depends on its ability to affect hindbrain neural circuits that control ingestive motor output. In this regard, anatomical, physiological, and behavioral data support the view that ingestive behavior outputs are modulated by neural signaling in the dorsal vagal complex (DVC), comprising the nucleus of the solitary tract, area postrema, and dorsal motor nucleus of the vagus. The DVC receives relayed and direct synaptic input from olfactory, glossopharyngeal, facial, trigeminal, vagal, and spinal viscerosensory afferents that convey information about the chemical and mechanical properties of food. Medial portions of the DVC contain fenestrated capillaries that provide local parenchymal access to blood-borne factors (e.g., toxins, cytokines, hormones, osmolytes) that affect food intake. DVC neurons are interconnected with brain stem central pattern generator, premotor, and motor nuclei that organize and execute ingestive movements such as licking, biting, chewing, and swallowing (3–5, 15, 17). DVC neurons also control parasympathetic outflow to the digestive tract (1). By determining the way in which ingesta are handled and metabolically processed, DVC circuits can help shape the viscerosensory landscape and thereby influence the occurrence and potency of many direct and indirect controls of food intake (14).A relatively small number of neurons lying within the caudal DVC and adjacent reticular formation are immunoreactive for glucagon-like peptide-1 (GLP-1) (9). These discretely localized neurons give rise to axonal projections that terminate within multiple regions of the brain stem, hypothalamus, and limbic forebrain where GLP-1 receptors are coexpressed. Importantly, hindbrain GLP-1 neurons appear to provide the sole source of endogenous ligand for these receptors, whose neuroanatomical localization suggests a potential functional role in the central control of food intake. Indeed, exogenous GLP-1 inhibits food intake in rats after central infusion into the lateral, third, or fourth ventricle, and in each case the anorexic effect of synthetic peptide is reversed by pharmacological antagonism of central GLP-1 receptors (2, 7, 12, 16, 18). Whereas such studies clearly indicate that synthetic GLP-1 can interact with endogenous receptors to inhibit food intake, they do not reveal whether endogenous GLP-1 signaling mechanisms actually participate in feeding control.This issue has been addressed, to some extent, by studies demonstrating that the majority of GLP-1-immunopositive neurons within the DVC are activated to express the immediate-early gene product c-Fos in experimental models of anorexia, including central administration of oxytocin (OT) (12), systemic administration of lithium chloride (LiCl), cholecystokinin octapeptide, or lipopolysaccharide (LPS) (11), and gastric balloon distension (19). Conversely, GLP-1 neurons do not express c-Fos in rats sated by voluntary consumption of a large meal (11), although food intake also is inhibited in this situation. Together these findings suggest that GLP-1 neurons are selectively activated by stimuli associated with visceral malaise and stress but not by stimuli associated with normal satiety. Moreover, the ability of central OT and systemic LiCl to inhibit food intake in rats is attenuated by pharmacological blockade of central GLP-1 receptors (10, 12, 13), evidence that endogenous GLP-1 signaling pathways are an important component of the neural circuits that mediate anorexic responses to these treatments. Similarly, Grill and colleagues (6) report in this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology that anorexia in rats after systemic LPS treatment is blunted significantly by pharmacological antagonism of central GLP-1 receptors, providing additional evidence for a specific role of GLP-1 signaling pathways in stress-induced anorexia. The authors also report that central antagonism of GLP-1 receptors by itself does not affect baseline food intake, thereby discounting a fundamental role for these pathways in normal satiety mechanisms.A brain stem receptor site of action for GLP-1 to inhibit food intake has been suggested based on the anorexic effect of synthetic peptide infused into the fourth ventricle (7). However, synthetic GLP-1 also inhibits food intake when infused directly into the hypothalamus in small doses (8) that are subthreshold for inhibiting food intake when infused into the lateral, third, or fourth ventricles. Thus it appears that exogenously administered GLP-1 can act at multiple levels of the central nervous system to inhibit food intake. It is important to note, however, that previous studies have not examined potential sites of action for endogenously released GLP-1 to suppress feeding. Grill and colleagues report that the anorexic effect of LPS treatment in rats is attenuated by blockade of GLP-1 receptors that are accessible from the fourth ventricle. Conversely, when the cerebral aqueduct is occluded to prevent concurrent antagonism of hindbrain receptors, LPS anorexia is unaffected by blockade of GLP-1 receptors accessible from the third ventricle (6). As the authors point out, their results highlight a potential role of hindbrain GLP-1 receptors in the inhibition of feeding produced by LPS treatment and minimize potential roles for hypothalamic and other forebrain GLP-1 receptors in this behavioral response.These new findings support the view that GLP-1 signaling pathways contained within the caudal brain stem contribute importantly to the anorexic effect of systemic LPS, an experimental model of acute inflammatory response and sickness behavior. Known direct and relayed projections from the DVC to somatic and autonomic motor nuclei provide potential routes by which brain stem GLP-1 signaling pathways might exert control over both the ingestion and digestion of food. The DVC is the major brain stem relay center for viscerosensory inputs to the brain and is also the recipient of direct descending projections from the hypothalamus and limbic forebrain. Thus the DVC and its resident GLP-1 neurons are well positioned to integrate interoceptive signals with cognitive/emotional state and thereby participate in context-specific modulation of food intake. The new data reported by Grill and colleagues invite continued focus on the DVC and its GLP-1-containing projections as integral components of the central neural circuits that shape ingestive behavior.REFERENCES1 Berthoud HR. Multiple neural systems controlling food intake and body weight. Neurosci Biobehav Rev 26: 393–428, 2002.Crossref | PubMed | ISI | Google Scholar2 Donahey JC, van-Dink G, Woods SC, and Seeley RJ. Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats. Brain Res 779: 75–83, 1998.Crossref | PubMed | ISI | Google Scholar3 Fay RA and Norgren R. Identification of rat brainstem multisynaptic connections to the oral motor nuclei in the rat using pseudorabies virus. I Masticatory muscle motor systems. 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J Neurosci 22: 10470–10475, 2002.Crossref | PubMed | ISI | Google Scholar8 McMahon LR and Wellman PJ. PVN infusion of GLP-1-(7–36) amide suppresses feeding but does not induce aversion or alter locomotion in rats. Am J Physiol Regul Integr Comp Physiol 274: R23–R29, 1998.Link | ISI | Google Scholar9 Merchenthaler I, Lane M, and Shughrue P. Distribution of pre-pro-glucagon and glucagon-like peptide-1 receptor messenger RNAs in the rat central nervous system. J Comp Neurol 403: 261–280, 1999.Crossref | PubMed | ISI | Google Scholar10 Rinaman L. A functional role for central glucagon-like peptide-1 receptors in lithium chloride-induced anorexia. Am J Physiol Regul Integr Comp Physiol 277: R1537–R1540, 1999.Link | ISI | Google Scholar11 Rinaman L. Interoceptive stress activates glucagon-like peptide-1 neurons that project to the hypothalamus. Am J Physiol Regul Integr Comp Physiol 277: R582–R590, 1999.Link | ISI | Google Scholar12 Rinaman L and Rothe EE. GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats. Am J Physiol Regul Integr Comp Physiol 283: R99–R106, 2002.Link | ISI | Google Scholar13 Seeley RJ, Blake K, Rushing PA, Benoit W, Eng J, Woods SC, and D'Alessio D. The role of CNS glucagon-like peptide-1 (7–36) amide receptors in mediating the visceral illness effects of lithium chloride. J Neurosci 20: 1616–1621, 2000.Crossref | PubMed | ISI | Google Scholar14 Smith GP. The controls of eating: a shift from nutritional homeostasis to behavioral neuroscience. Nutrition 16: 814–820, 2000.Crossref | PubMed | ISI | Google Scholar15 Streefland C and Jansen K. Intramedullary projections of the rostral nucleus of the solitary tract in the rat: gustatory influences on autonomic output. Chem Senses 24: 655–664, 1999.Crossref | PubMed | ISI | Google Scholar16 Tang-Christensen M, Larsen PJ, Goke R, Fink-Jensen A, Jessop DS, Moller M, and Sheikh SP. Central administration of GLP-1-(7–36) amide inhibits food and water intake in rats. Am J Physiol Regul Integr Comp Physiol 271: R848–R856, 1996.Link | ISI | Google Scholar17 Travers JB and Rinaman L. Identification of lingual motor control circuits using two strains of pseudorabies virus. Neuroscience 115: 1139–1151, 2002.Crossref | PubMed | ISI | Google Scholar18 Turton MD, O'Shea D, Gunn I, Beak SA, Edwards CM, Meeran K, Choi SJ, Taylor GM, Heath MM, Lambert PD, Wilding JP, Smith DM, Ghatei MA, Herbert J, and Bloom SR. A role for glucagon-like peptide-1 in the central regulation of feeding. Nature 379: 69–72, 1996.Crossref | PubMed | ISI | Google Scholar19 Vrang N, Phifer CB, Corkern MM, and Berthoud HR. Gastric distension induces c-Fos in medullary GLP-1/2-containing neurons. Am J Physiol Regul Integr Comp Physiol 285: R470–R478, 2003.Link | ISI | Google Scholar20 Watts AG. Understanding the neural control of ingestive behaviors: helping to separate cause from effect with dehydration-associated anorexia. Horm Behav 37: 261–283, 2000.Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: L. Rinaman, Dept. of Neuroscience, Univ. of Pittsburgh, 446 Crawford Hall, Pittsburgh, PA 15260 (E-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByVagal Interoceptive Modulation of Motivated BehaviorJ. W. Maniscalco, and L. Rinaman7 February 2018 | Physiology, Vol. 33, No. 2Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGBRobert E. Steinert, Christine Feinle-Bisset, Lori Asarian, Michael Horowitz, Christoph Beglinger, and Nori Geary21 December 2016 | Physiological Reviews, Vol. 97, No. 1Appetite controlled by a cholecystokinin nucleus of the solitary tract to hypothalamus neurocircuit14 March 2016 | eLife, Vol. 5Early life experience shapes the functional organization of stress-responsive visceral circuitsPhysiology & Behavior, Vol. 104, No. 4Hindbrain noradrenergic A2 neurons: diverse roles in autonomic, endocrine, cognitive, and behavioral functionsLinda Rinaman1 February 2011 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 300, No. 2Proteins Activate Satiety-Related Neuronal Pathways in the Brainstem and Hypothalamus of RatsThe Journal of Nutrition, Vol. 138, No. 6 More from this issue > Volume 287Issue 5November 2004Pages R1035-R1036 Copyright & PermissionsCopyright © 2004 the American Physiological Societyhttps://doi.org/10.1152/ajpregu.00437.2004PubMed15475502History Published online 1 November 2004 Published in print 1 November 2004 Metrics" @default.
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