NDLI: Constraint-induced movement therapy overcomes the intrinsic axonal growth-inhibitory signals in stroke rats.

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Constraint-induced movement therapy overcomes the intrinsic axonal growth-inhibitory signals in stroke rats.

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Constraint-induced movement therapy overcomes the intrinsic axonal growth-inhibitory signals in stroke rats.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhao, Shanshan Jolkkonen, Jukka Zhao, Mei Zhao, Chuansheng Xiao, Ting
Description	Author Affiliation: Zhao S ( Department of Neurology, The First Hospital of China Medical University, Shenyang, Liaoning, PR China.)
Abstract	BACKGROUND AND PURPOSE: Constraint-induced movement therapy (CIMT) improves functional outcome in patients with stroke possibly through structural plasticity. We hypothesized that CIMT could enhance axonal growth by overcoming the intrinsic growth-inhibitory signals, leading eventually to improved behavioral performance in stroke rats. METHODS: Focal cerebral ischemia was induced by intracerebral injection of endothelin-1. Adult Wistar rats were divided into a sham-operated group, an ischemic group, and an ischemic group treated with CIMT. CIMT started at postoperative day 7 and continued for 3 weeks. Biotinylated dextran amine was injected into the contralateral sensorimotor cortex at postoperative day 14 to trace crossing axons at the cervical spinal cord. The expressions of Nogo-A, Nogo receptor, RhoA, and Rho-associated kinase in the peri-infarct cortex, and the expressions of biotinylated dextran amine, growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated spinal cord were measured by immunohistochemistry and Western blots. Behavioral recovery was analyzed at postoperative days 29 to 32. RESULTS: Infarct volumes were not different between groups after stroke. CIMT significantly increased the length and the number of midline crossings of contralateral corticospinal axons to the denervated cervical spinal cord. CIMT significantly decreased the expressions of Nogo-A/Nogo receptor and RhoA/Rho-associated kinase in the peri-infarct cortex, and increased the expressions of growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated cervical spinal cord. Behavioral performances assessed by the beam-walking test and the water maze test were improved significantly by CIMT. CONCLUSIONS: CIMT promoted poststroke synaptic plasticity and axonal growth at least partially by overcoming the intrinsic growth-inhibitory signaling, leading to improved behavioral outcome.
ISSN	00392499
e-ISSN	15244628
Journal	Stroke
Issue Number	6
Volume Number	44
Language	English
Publisher	Lippincott Williams & Wilkins (on behalf of the American Heart Association)
Publisher Date	2013-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Axons Physiology Movement Physical Therapy Modalities Restraint, Physical Signal Transduction Stroke Physiopathology Therapy Animals Pathology Disease Models, Animal Endothelin-1 Adverse Effects Gap-43 Protein Metabolism Gpi-linked Proteins Injections, Intraventricular Myelin Proteins Neuronal Plasticity Rats, Wistar Receptors, Cell Surface Chemically Induced Synaptophysin Rhoa Gtp-binding Protein Research Support, Non-u.s. Gov't Discipline Cardiology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Advanced and Specialized Nursing Neurology (clinical)

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