Document Detail


From hunger to satiety: reconfiguration of a feeding network by Aplysia neuropeptide Y.
MedLine Citation:
PMID:  17392465     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A shift in motivational state often produces behavioral change, but the underlying mechanisms are poorly understood. In the marine mollusc, Aplysia californica, feeding-induced transition from a hunger to satiation state leads to a slowdown and an eventual termination of feeding. Because the multifunctional feeding network generates both ingestion and the competing response, egestion, it is possible that the transition from a hunger to a satiety state is associated with network reconfiguration that results in production of fewer ingestive and more egestive responses. Chronic electrophysiological recordings in free-feeding Aplysia showed that as the meal progressed, food elicited fewer ingestive responses and simultaneously increased the number of egestive responses. Injections of Aplysia neuropeptide Y (apNPY) reduced food intake and slowed down the rate of ingestion. apNPY was localized to buccal-ganglion afferents originating in the gut-innervating esophageal nerve (EN), a nerve involved both in satiation and in the generation of egestive programs. During EN stimulation, apNPY was released in the feeding circuit. Importantly, stimulation of the cerebral-buccal interneuron-2, a command-like interneuron that is activated by food and normally elicits ingestive responses, elicited egestive responses in the presence of apNPY. This was accompanied by increased activity of the egestion-promoting interneuron B20 and decreased activity in the ingestion-promoting interneuron B40. Thus, apNPYergic reconfiguration of the feeding central pattern generator plays a role in the gradual transition from hunger to satiety states. More generally, changes in the motivational states may involve not only simple network inhibition but may also require network reconfiguration.
Authors:
Jian Jing; Ferdinand S Vilim; Charles C Horn; Vera Alexeeva; Nathan G Hatcher; Kosei Sasaki; Irene Yashina; Yuriy Zhurov; Irving Kupfermann; Jonathan V Sweedler; Klaudiusz R Weiss
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  27     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-29     Completed Date:  2007-04-24     Revised Date:  2013-07-26    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3490-502     Citation Subset:  IM    
Affiliation:
Department of Neuroscience, Mount Sinai School of Medicine, New York, New York 10029, USA. Jian.Jing@mssm.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Aplysia / physiology*
Cheek / physiology
Feeding Behavior / physiology
Ganglia, Invertebrate / metabolism
Hunger / physiology*
Immunohistochemistry
Male
Motivation
Neurons / metabolism
Neuropeptide Y / metabolism*,  pharmacology
Rats
Rats, Sprague-Dawley
Satiety Response / physiology*
Grant Support
ID/Acronym/Agency:
DA 13330/DA/NIDA NIH HHS; F32 MH011586/MH/NIMH NIH HHS; MH 035564/MH/NIMH NIH HHS; P30 DA 018310/DA/NIDA NIH HHS; R01 MH 50235/MH/NIMH NIH HHS; R01 NS 031609/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Neuropeptide Y

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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