Document Detail

Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity.
MedLine Citation:
PMID:  16580138     Owner:  NLM     Status:  MEDLINE    
Synaptic plasticity and behaviors are likely dependent on the capacity of neurons to meet the energy demands imposed by neuronal activity. We used physical activity, a paradigm intrinsically associated with energy consumption/expenditure and cognitive enhancement, to study how energy metabolism interacts with the substrates for neuroplasticity. We found that in an area critical for learning and memory, the hippocampus, exercise modified aspects of energy metabolism by decreasing oxidative stress and increasing the levels of cytochrome c oxidase-II, a specific component of mitochondrial machinery. We infused 1,25-dihydroxyvitamin D3, a modulator of energy metabolism, directly into the hippocampus during 3 days of voluntary wheel running and measured its effects on brain-derived neurotrophic factor-mediated synaptic plasticity. Brain-derived neurotrophic factor is a central player for the effects of exercise on synaptic and cognitive plasticity. We found that 25-dihydroxyvitamin D3 decreased exercise-induced brain-derived neurotrophic factor but had no significant effect on neurotrophin-3 levels, thereby suggesting a level of specificity for brain-derived neurotrophic factor in the hippocampus. 25-Dihydroxyvitamin D3 injection also abolished the effects of exercise on the consummate end-products of brain-derived neurotrophic factor action, i.e. cyclic AMP response element-binding protein and synapsin I, and modulated phosphorylated calmodulin protein kinase II, a signal transduction cascade downstream to brain-derived neurotrophic factor action that is important for learning and memory. We also found that exercise significantly increased the expression of the mitochondrial uncoupling protein 2, an energy-balancing factor concerned with ATP production and free radical management. Our results reveal a fundamental mechanism by which key elements of energy metabolism may modulate the substrates of hippocampal synaptic plasticity.
S Vaynman; Z Ying; A Wu; F Gomez-Pinilla
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2006-03-31
Journal Detail:
Title:  Neuroscience     Volume:  139     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2006  
Date Detail:
Created Date:  2006-05-08     Completed Date:  2006-07-26     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1221-34     Citation Subset:  IM    
Department of Physiological Science, UCLA, Los Angeles, CA 90095, USA.
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MeSH Terms
Analysis of Variance
Brain-Derived Neurotrophic Factor / physiology*
CREB-Binding Protein / genetics,  metabolism
Calcitriol / pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases / metabolism
Cyclooxygenase 2 / metabolism
Energy Metabolism / drug effects*,  physiology
Hippocampus / cytology
Ion Channels
Membrane Transport Proteins / metabolism
Mitochondrial Proteins / metabolism
Neuronal Plasticity / drug effects*
Neurons / drug effects*
Physical Conditioning, Animal / methods
RNA, Messenger / metabolism
Random Allocation
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction / methods
Synapsins / metabolism
Time Factors
Vitamins / pharmacology
Grant Support
Reg. No./Substance:
0/Brain-Derived Neurotrophic Factor; 0/Ion Channels; 0/Membrane Transport Proteins; 0/Mitochondrial Proteins; 0/RNA, Messenger; 0/Synapsins; 0/Vitamins; 0/mitochondrial uncoupling protein 2; 32222-06-3/Calcitriol; EC 2; EC protein, rat; EC Protein; EC Protein Kinase Type 2; EC Protein Kinases

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

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