European Journal of Neuroscience, Sept, 2012, Vol.36, p.2632(8)
To purchase or authenticate to the full-text of this article, please visit this link: http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2012.08174.x/abstract Byline: Jan A. Jablonka(1)(2), Malgorzata Kossut(2), Otto W. Witte(3), Monika Liguz-Lecznar(2) Keywords: 2DG; inflammation; plasticity; rat; somatosensory cortex Abstract Despite indications that brain plasticity may be enhanced after stroke, we have described impairment of experience-dependent plasticity in rat cerebral cortex neighboring the stroke-induced lesion. Photothrombotic stroke was centered behind the barrel cortex in one cerebral hemisphere of rats. Plasticity of cortical representation of one row of vibrissae was induced by sensory deprivation of all surrounding whiskers for 1 month, and visualized with [.sub.14C]-2-deoxyglucose autoradiography. In control rats deprivation resulted in an enlargement of functional cortical representation of the spared row of vibrissae. After a focal stroke neighbouring the barrel cortex, no plasticity of the spared row representation was found. Investigation of plastic changes with deprivation initiated 1 week and 1 month after stroke have shown that later poststroke onset of deprivation resulted in a partial recovery of cortical plasticity in the barrel field. Western blot analysis of proinflammatory enzyme cyclooxygenase-2 (COX-2) expression revealed its strong upregulation in the barrel cortex 24 h after stroke. When chronic treatment with the anti-inflammatory drug ibuprofen (10 mg/kg or 20 mg/kg) accompanied deprivation, plasticity was restored. Ibuprofen applied before the ischemia also prevented the poststroke upregulation of COX-2. The results strongly suggest that poststroke impairment of experience-dependent cortical plasticity is caused by stroke-induced inflammatory reactions that subside with poststroke delay and can be at least partially ameliorated by pharmacological treatment. Author Affiliation: (1)Department of Animal Physiology, Faculty of Biology, Warsaw University, Warsaw, Poland (2)Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Warsaw, Poland (3)Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany Correspondence: (*) Malgorzata Kossut, as above. E-mail: firstname.lastname@example.org Received 17 November 2011, revised 27 April 2012, accepted 30 April 2012
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