Document Detail

Food-elicited increases in cortical acetylcholine release require orexin transmission.
MedLine Citation:
PMID:  17928158     Owner:  NLM     Status:  MEDLINE    
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.
D Frederick-Duus; M F Guyton; J Fadel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-09-11
Journal Detail:
Title:  Neuroscience     Volume:  149     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-10-30     Completed Date:  2008-01-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  499-507     Citation Subset:  IM    
Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29208, USA.
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MeSH Terms
Acetylcholine / metabolism*
Benzoxazoles / pharmacology
Cerebral Cortex / injuries,  metabolism*
Food Deprivation / physiology
Hypothalamic Hormones / physiology
Intracellular Signaling Peptides and Proteins / physiology*
Melanins / physiology
Neuropeptides / physiology*
Pituitary Hormones / physiology
Prosencephalon / injuries,  physiology
Rats, Inbred F344
Receptors, G-Protein-Coupled / antagonists & inhibitors,  genetics,  physiology
Receptors, Neuropeptide / antagonists & inhibitors,  genetics,  physiology
Synaptic Transmission / physiology*
Urea / analogs & derivatives,  pharmacology
Reg. No./Substance:
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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