Document Detail

De novo neurogenesis in adult hypothalamus as a compensatory mechanism to regulate energy balance.
MedLine Citation:
PMID:  20071537     Owner:  NLM     Status:  MEDLINE    
The ability to develop counter-regulatory mechanisms to maintain energy balance in response to environmental and physiologic insults is essential for survival, but the mechanisms underlying these compensatory regulations are poorly understood. Agouti-related peptide (AGRP) and Neuropeptide Y are potent orexigens and are coexpressed in neurons in the arcuate nucleus of the hypothalamus. Acute ablation of these neurons leads to severe anorexia and weight loss, whereas progressive degeneration of these neurons has minimal impact on food intake and body weight, suggesting that compensatory mechanisms are developed to maintain orexigenic drive. In this study, we show that cell proliferation is increased in the hypothalamus of adult mutant animals in which AgRP neurons undergo progressive neurodegeneration due to deletion of mitochondrial transcription factor A, and that a subset of these newly generated cells differentiate into AgRP neurons along with other resident neuronal subtypes. Furthermore, some of the newly generated cells are capable of responding to leptin, and a central blockade of cell proliferation in adult animals results in decreases in food intake and body adiposity in mutant but not in control animals. Our study indicates that neurons important for energy homeostasis can be regenerated in adult feeding centers under neurodegenerative conditions. It further suggests that de novo neurogenesis might serve as a compensatory mechanism contributing to the plastic control of energy balance in response to environmental and physiologic insults.
Andrew A Pierce; Allison W Xu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  30     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-14     Completed Date:  2010-02-01     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  723-30     Citation Subset:  IM    
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MeSH Terms
Absorptiometry, Photon / methods
Adrenocorticotropic Hormone / metabolism
Agouti-Related Protein / genetics
Analysis of Variance
Animals, Newborn
Antimetabolites, Antineoplastic / pharmacology
Body Composition / drug effects,  genetics
Body Weight / drug effects,  genetics
Bromodeoxyuridine / metabolism
Cell Count / methods
Cell Proliferation / drug effects
Cytarabine / pharmacology
Eating / drug effects,  genetics
Energy Metabolism / drug effects,  genetics,  physiology*
Hypothalamus / cytology,  physiology*
Injections, Intraventricular / methods
Ki-67 Antigen / metabolism
Mice, Transgenic
Mutation / genetics
Neurogenesis / physiology*
Neurons / metabolism,  physiology*
Proliferating Cell Nuclear Antigen / metabolism
STAT3 Transcription Factor / metabolism
Time Factors
Grant Support
Reg. No./Substance:
0/Agouti-Related Protein; 0/Agrp protein, mouse; 0/Antimetabolites, Antineoplastic; 0/Ki-67 Antigen; 0/Proliferating Cell Nuclear Antigen; 0/STAT3 Transcription Factor; 04079A1RDZ/Cytarabine; 9002-60-2/Adrenocorticotropic Hormone; G34N38R2N1/Bromodeoxyuridine

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

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