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(Stroke. 2004;35:e346.)
© 2004 American Heart Association, Inc.
Research Reports |
From the Yamaguchi University School of Medicine (H.F.), Ube, Yamaguchi, Japan; the Neurobionics Group (H.F., H.K., S.S.S.), Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology (AIST); and the Research Center for Advanced Science and Technology (H.F.), Graduate School of Information Science and Technology and Graduate School of Medicine (K.M.), The University of Tokyo, Japan.
Correspondence to Dr H. Fujioka, 3-6-11, Ozuki-Chaya, Shimonoseki, Yamaguchi, 750-1144, Japan. E-mail e909eb{at}yamaguchi-u.ac.jp
Background and Purpose This article addresses how neuroplastic changes are initiated after an ischemic stroke.
Methods A focal cerebral ischemia was photochemically induced on the primary somatosensory cortex of rats, and in vivo electrophysiological recordings were performed on the peri-infarct cortex before and from 1 to 6 hours after the infarction.
Results Paired-pulse analysis of evoked field potentials to peripheral electrical stimuli showed statistically significant neuronal hyperexcitability that was associated with rapid expansion of receptive fields (146.1% at 1 hour and 553.6% at 6 hours) as early as 1 hour after the infarction (P<0.05). Current source density analysis revealed increased current sinks in cortical layer II/III.
Conclusions Our electrophysiological results showed, for the first time to our knowledge, rapid plastic changes in the peri-infarct cortex during the hyperacute stage of an ischemic stroke. Manipulation of this rapid plasticity may affect subsequent plastic changes.
Key Words: cerebral ischemia neuronal plasticity somatosensory evoked potentials rats electrophysiology
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