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Brain Res. 2010 Sep 2;1350:18-34. doi: 10.1016/j.brainres.2010.03.059. Epub 2010 Mar 27.

Ascending projections from the caudal visceral nucleus of the solitary tract to brain regions involved in food intake and energy expenditure.

Author information

  • Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA. rinaman@pitt.edu

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.

2010 Elsevier B.V. All rights reserved.

PMID:
20353764
[PubMed - indexed for MEDLINE]
PMCID:
PMC2909454
Free PMC Article

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