Document Detail


Exercise can increase small heat shock proteins (sHSP) and pre- and post-synaptic proteins in the hippocampus.
MedLine Citation:
PMID:  19014914     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The molecular events mediating the complex interaction between exercise and cognition are not well-understood. Although many aspects of the signal transduction pathways mediate exercise induced improvement in cognition are elucidated, little is known about the molecular events interrelating physiological stress with synaptic proteins, following physical exercise. Small heat shock proteins (sHSP), HSP27 and alpha-B-crystallin are co-localized to synapses and astrocytes, but their role in the brain is not well-understood. We investigated whether their levels in the hippocampus were modulated by exercise, using a well characterized voluntary exercise paradigm. Since sHSP are known to be regulated by many intracellular signaling molecules in other cells types outside the brain, we investigated whether similar regulation may serve a role in the brain by measuring protein kinase B (PKB/Akt), pGSK3 and the mitogen activated protein (MAP) kinases, p38, phospho-extracellular signal-regulated kinase (pERK) and phospho-c-Jun kinase (pJNK). Results demonstrated exercise-dependent increases in HSP27 and alpha-B-crystallin levels. We observed that increases in sHSP coincided with robust elevations in the presynaptic protein, SNAP25 and the post-synaptic proteins NR2b and PSD95. Exercise had a differential impact on kinases, significantly reducing pAkt and pERK, while increasing p38 MAPK. In conclusion, we demonstrate four early novel hippocampal responses to exercise that have not been identified previously: the induction of (1) sHSPs (2) the synaptic proteins SNAP-25, NR2b, and PSD-95, (3) the MAP kinase p38 and (4) the immediate early gene product MKP1. We speculate that sHSP may play a role in synaptic plasticity in response to exercise.
Authors:
Shuxin Hu; Zhe Ying; Fernando Gomez-Pinilla; Sally Ann Frautschy
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2008-11-05
Journal Detail:
Title:  Brain research     Volume:  1249     ISSN:  1872-6240     ISO Abbreviation:  Brain Res.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-01-06     Completed Date:  2009-01-30     Revised Date:  2014-09-15    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  191-201     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Blotting, Western
Extracellular Signal-Regulated MAP Kinases / metabolism
Glial Fibrillary Acidic Protein / metabolism
HSP27 Heat-Shock Proteins / metabolism*
Hippocampus / physiology*
Intracellular Signaling Peptides and Proteins / metabolism
Linear Models
MAP Kinase Signaling System
Male
Membrane Proteins / metabolism
Physical Conditioning, Animal / physiology*
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate / metabolism
Signal Transduction
Synapses / metabolism*
Synaptosomal-Associated Protein 25 / metabolism
alpha-Crystallin B Chain / metabolism*
Grant Support
ID/Acronym/Agency:
AG021975/AG/NIA NIH HHS; NS50465/NS/NINDS NIH HHS; R01 AG010685/AG/NIA NIH HHS; R01 AG010685-14/AG/NIA NIH HHS; R01 AG016793/AG/NIA NIH HHS; R01 AG016793-05/AG/NIA NIH HHS; R01 AG021975/AG/NIA NIH HHS; R01 AG021975-05/AG/NIA NIH HHS; R01 NS050465/NS/NINDS NIH HHS; R01 NS050465-04/NS/NINDS NIH HHS; R01 NS056413/NS/NINDS NIH HHS; R01 NS056413-01A2/NS/NINDS NIH HHS; U01 AG028583/AG/NIA NIH HHS; U01 AG028583-04/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Dlgh4 protein, rat; 0/Glial Fibrillary Acidic Protein; 0/HSP27 Heat-Shock Proteins; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Proteins; 0/Receptors, N-Methyl-D-Aspartate; 0/Snap25 protein, rat; 0/Synaptosomal-Associated Protein 25; 0/alpha-Crystallin B Chain; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases
Comments/Corrections

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