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Rinaman L. Ascending projections from the caudal visceral nucleus of the solitary tract to brain regions involved in food intake and energy expenditure. Brain Res 1350: 18-34

Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Brain research (Impact Factor: 2.83). 03/2010; 1350:18-34. DOI: 10.1016/j.brainres.2010.03.059
Source: PubMed

ABSTRACT Metabolic homeostasis reflects the complex output of endocrine, autonomic, and behavioral control circuits that extend throughout the central nervous system. Brain regions that control food intake and energy expenditure are privy to continuous visceral sensory feedback signals that presumably modulate appetite, satiety, digestion, and metabolism. Sensory signals from the gastrointestinal tract and associated digestive viscera are delivered to the brain primarily by vagal afferents that terminate centrally within the caudal nucleus of the solitary tract (NST), with signals subsequently relayed to higher brain regions by parallel noradrenergic and peptidergic projection pathways arising within the NST. This article begins with an overview of these ascending pathways identified in adult rats using a standard anterograde tracer microinjected into the caudal visceral sensory region of the NST, and also by immunocytochemical localization of glucagon-like peptide-1. NST projection targets identified by these two approaches are compared to the distribution of neurons that become infected after inoculating the ventral stomach wall with a neurotropic virus that transneuronally infects synaptically-linked chains of neurons in the anterograde (i.e., ascending sensory) direction. Although the focus of this article is the anatomical organization of axonal projections from the caudal visceral NST to the hypothalamus and limbic forebrain, discussion is included regarding the hypothesized role of these projections in modulating behavioral arousal and coordinating endocrine and behavioral (i.e., hypophagic) responses to stress.

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    • "Control of food intake in the brain is regulated by the integration of both the neuronal and humoral signals from the periphery. A variety of sensory information derived from the gastrointestinal tract is transmitted to the nucleus of the tractus solitaries (NTS) in the medulla oblongata via the vagal afferent nerve, terminating in hypothalamic nuclei implicated in the control of feeding (Rinaman 2010). The nodose ganglion, located outside the jugular foramen, is a constellation of vagal afferent neurons that synthesize receptors for gut peptides that regulate feeding and energy homeostasis (Zhuo et al. 1997, Konturek et al. 2004). "
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    ABSTRACT: Ghrelin, a stomach-derived orexigenic peptide, transmits starvation signals to the hypothalamus via the vagus afferent nerve. Peripheral administration of ghrelin does not induce food intake in high fat diet (HFD)-induced obese mice. We investigated whether this ghrelin resistance was caused by dysfunction of the vagus afferent pathway. Subcutaneous ghrelin administration did not induce food intake, suppression of oxygen consumption, electrical activity of the vagal afferent nerve, phosphorylation of extracellular-signal-regulated kinases 2 (ERK2) and AMP-activated protein kinase α (AMPKα) in the nodose ganglion, or Fos expression in hypothalamic arcuate nucleus of mice fed a HFD for 12 weeks. Administration of anti-ghrelin IgG did not induce suppression of food intake in HFD-fed mice. Expression levels of ghrelin receptor mRNA in the nodose ganglion and hypothalamus of HFD-fed mice were reduced. Inflammatory responses, including upregulation of macrophage/microglia markers and inflammatory cytokines, occurred in the nodose ganglion and hypothalamus of HFD-fed mice. A high-fat diet blunted ghrelin signaling in the nodose ganglion via a mechanism involving in situ activation of inflammation. These results show that ghrelin resistance in the obese state may be caused by dysregulation of ghrelin signaling via the vagal afferent.
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    • "Recently , it has been demonstrated that DMV is a part of the dorsal motor complex, composed the nucleus tractus solitarii (NTS) and area postrema (Wang et al. 2014). NTS projects to many brain areas including the hindbrain, midbrain and forebrain, and dopamine-related brain structures—the ventral tegmental area (VTA) and nucleus accumbens (NAC) (Merchenthaler et al. 1999; Rinaman 2010). In addition, the vagus nerve connects the DMV with, among others, the gastrointestinal system, which is considered to be significantly affected at the onset of PD, even before motor signs occur (Braak et al. 2003). "
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    • "By contrast, killing POMC neurons induces hyperphagia and obesity (Yaswen et al., 1999; Coll et al., 2004; Xu et al., 2005; Zhan et al., 2013), whereas ablating AgRP neurons in adult mice induces hypophagia and, ultimately, starvation (Gropp et al., 2005; Luquet et al., 2005). Classic tract tracings have revealed that neurons in the ARC and NTS receive inputs from, and project to, broad brain areas (Makara and Hodacs, 1975; Ricardo and Koh, 1978; Schwaber et al., 1982; Chronwall, 1985; Gruber et al., 1987; Sim and Joseph, 1991; Magoul et al., 1993; Rinaman, 2010). Different cell types are intermingled in both brain areas, thus making it impossible to assign conventional tracing results to specific types of neurons among nuclei. "
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