Next Article in Journal
Catalytic Conversion of Cellulose to Levulinic Acid by Metal Chlorides
Next Article in Special Issue
Neuroscientists as Cartographers: Mapping the Crossroads of Gonadal Hormones, Memory and Age Using Animal Models
Previous Article in Journal
Photochemistry of Flavonoids
Previous Article in Special Issue
Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms
Article Menu

Article Versions

Export Article

Open AccessArticle
Molecules 2010, 15(8), 5246-5257; doi:10.3390/molecules15085246

Pre-Ischemic Treadmill Training Induces Tolerance to Brain Ischemia: Involvement of Glutamate and ERK1/2

Department of Rehabilitation Medicine, Hua Shan Hospital, Fudan University, WuLuMuQi Middle Road 12, Shanghai 200040, China
Author to whom correspondence should be addressed.
Received: 14 July 2010 / Revised: 28 July 2010 / Accepted: 30 July 2010 / Published: 2 August 2010
(This article belongs to the Special Issue Neuroprotective Strategies)
Download PDF [237 KB, uploaded 18 June 2014]   |  


Physical exercise has been shown to be beneficial in stroke patients and animal stroke models. However, the exact mechanisms underlying this effect are not yet very clear. The present study investigated whether pre-ischemic treadmill training could induce brain ischemic tolerance (BIT) by inhibiting the excessive glutamate release and event-related kinase 1/2 (ERK1/2) activation observed in rats exposed to middle cerebral artery occlusion (MCAO). Sprague–Dawley rats were divided into three groups (n = 12/group): sham surgery without prior exercise, MCAO without prior exercise and MCAO following three weeks of exercise. Pre-MCAO exercise significantly reduced brain infarct size (103.1 ± 6.7 mm3) relative to MCAO without prior exercise (175.9 ± 13.5 mm3). Similarly, pre-MCAO exercise significantly reduced neurological defects (1.83 ± 0.75) relative to MCAO without exercise (3.00 ± 0.63). As expected, MCAO increased levels of phospho-ERK1/2 (69 ± 5%) relative to sham surgery (40 ± 5%), and phospho-ERK1/2 levels were normalized in rats exposed to pre-ischemic treadmill training (52 ± 6%) relative to MCAO without exercise (69% ± 5%). Parallel effects were observed on striatal glutamate overflow. This study suggests that pre-ischemic treadmill training might induce neuroprotection by inhibiting the phospho-ERK1/2 over-activation and reducing excessive glutamate release.
Keywords: ERK1/2; exercise-induced neuroprotection; glutamate; ischemia/reperfusion injury; microdialysis ERK1/2; exercise-induced neuroprotection; glutamate; ischemia/reperfusion injury; microdialysis

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Zhang, F.; Wu, Y.; Jia, J.; Hu, Y.-S. Pre-Ischemic Treadmill Training Induces Tolerance to Brain Ischemia: Involvement of Glutamate and ERK1/2. Molecules 2010, 15, 5246-5257.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top