| Food-elicited increases in cortical acetylcholine release require orexin transmission. | |
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MedLine Citation:
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PMID: 17928158 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The corticopetal basal forebrain cholinergic system (BFCS) is crucial for normal attentional function and cortical acetylcholine release is increased by stimuli with high motivational salience. Projections from the lateral hypothalamus to the basal forebrain have been previously described and have been hypothesized to relay interoceptive information to this area but little is known about the phenotypic and functional nature of hypothalamic modulation of the BFCS. We have previously shown that orexin (hypocretin) fibers from the hypothalamus distribute densely among basal forebrain choline acetyltransferase-positive neurons and that intrabasalis administration of orexin A increases cortical acetylcholine release. Here, we used in vivo microdialysis to test the hypothesis that the orexin system is necessary for activation of the BFCS in response to a food-related stimulus in food-restricted rats. Elimination of the majority of orexin neurons with the toxin orexin B-saporin significantly blunted the cholinergic response to presentation of palatable food in these animals. Similar effects were seen in animals acutely pretreated with the orexin 1 receptor antagonist, SB-334867, which also increased feeding latency. Collectively, these data suggest that orexin interactions with the BFCS may be a critical component of the neurobiological substrates by which interoceptive cues bias the allocation of attentional resources toward exteroceptive stimuli related to homeostatic challenges. |
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Authors:
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D Frederick-Duus; M F Guyton; J Fadel |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-09-11 |
Journal Detail:
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Title: Neuroscience Volume: 149 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 2007 Nov |
Date Detail:
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Created Date: 2007-10-30 Completed Date: 2008-01-16 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: United States |
Other Details:
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Languages: eng Pagination: 499-507 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29208, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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metabolism* Animals Benzoxazoles / pharmacology Cerebral Cortex / injuries, metabolism* Food* Food Deprivation / physiology Hypothalamic Hormones / physiology Immunohistochemistry Intracellular Signaling Peptides and Proteins / physiology* Male Melanins / physiology Microdialysis Neuropeptides / physiology* Pituitary Hormones / physiology Prosencephalon / injuries, physiology Rats Rats, Inbred F344 Receptors, G-Protein-Coupled / antagonists & inhibitors, genetics, physiology Receptors, Neuropeptide / antagonists & inhibitors, genetics, physiology Synaptic Transmission / physiology* Urea / analogs & derivatives, pharmacology |
| Chemical | |
Reg. No./Substance:
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0/1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea; 0/Benzoxazoles; 0/Hypothalamic Hormones; 0/Intracellular Signaling Peptides and Proteins; 0/Melanins; 0/Neuropeptides; 0/Pituitary Hormones; 0/Receptors, G-Protein-Coupled; 0/Receptors, Neuropeptide; 0/orexin receptors; 0/orexins; 51-84-3/Acetylcholine; 57-13-6/Urea; 67382-96-1/melanin-concentrating hormone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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