Document Detail


Long-term perturbation of spine plasticity results in distinct impairments of cognitive function.
MedLine Citation:
PMID:  22862288     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dendritic spines serve as the post-synaptic structural component of synapses. The structure and function of dendritic spines are dynamically regulated by a number of signaling pathways and allow for normal neural processing, whereas aberrant spine changes are thought to contribute to cognitive impairment in neuropsychiatric and neurodegenerative disorders. However, spine changes within different brain regions and their contribution to specific cognitive functions, especially later in adulthood, is not well understood. In this study, we used late-adult KALRN-deficient mice as a tool to investigate the vulnerability of different cognitive functions to long-term perturbations in spine plasticity in different forebrain regions. We found that in these mice, loss of one or both copies of KALRN lead to genotype and brain region-dependent reductions in spine density. Surprisingly, heterozygote and knockout mice showed differential impairments in cognitive phenotypes, including working memory, social recognition, and social approach. Correlation analysis between the site and magnitude of spine loss and behavioral alterations suggests that the interplay between brain regions is critical for complex cognitive processing and underscores the importance of spine plasticity in normal cognitive function. Long-term perturbation of spine plasticity results in distinct impairments of cognitive function. Using genetically modified mice deficient in a central regulator of spine plasticity, we investigated the brain region-specific contribution of spine numbers to various cognitive functions. We found distinct cognitive functions display differential sensitivity to spine loss in the cortex and hippocampus. Our data support spines as neuronal structures important for cognition and suggest interplay between brain regions is critical for complex cognitive processing.
Authors:
Jon-Eric Vanleeuwen; Peter Penzes
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-11
Journal Detail:
Title:  Journal of neurochemistry     Volume:  123     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-08     Completed Date:  2013-01-10     Revised Date:  2013-12-05    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  781-9     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors Journal of Neurochemistry © 2012 International Society for Neurochemistry.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / pathology*,  physiopathology
Cognition / physiology
Cognition Disorders / pathology*,  physiopathology*
Dendritic Spines / pathology*
Guanine Nucleotide Exchange Factors / deficiency,  genetics
Male
Mice
Mice, Knockout
Neuronal Plasticity / physiology*
Grant Support
ID/Acronym/Agency:
1F31MH087043/MH/NIMH NIH HHS; R01 MH071316/MH/NIMH NIH HHS; R01 MH097216/MH/NIMH NIH HHS; R01MH071316/MH/NIMH NIH HHS; R01MH097216/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Guanine Nucleotide Exchange Factors; 0/kalirin protein, mouse
Comments/Corrections

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