PMID- 23219910 OWN - NLM STAT- MEDLINE DCOM- 20130725 LR - 20130129 IS - 1873-7544 (Electronic) IS - 0306-4522 (Linking) VI - 231 DP - 2013 Feb 12 TI - Ipsilateral versus contralateral spontaneous post-stroke neuroplastic changes: involvement of BDNF? PG - 169-81 LID - S0306-4522(12)01165-7 [pii] LID - 10.1016/j.neuroscience.2012.11.054 [doi] AB - Stroke is a leading cause of death and disability in industrialized countries. Although surviving patients exhibit a certain degree of restoration of function attributable to brain plasticity, the majority of stroke survivors has to struggle with persisting deficits. In order to potentiate post-stroke recovery, several rehabilitation therapies have been undertaken and many experimental studies have reported that brain-derived neurotrophic factor (BDNF) is central to many facets of neuroplastic processes. However, although BDNF role in brain plasticity is well characterized through strategies that manipulate its content, the involvement of this neurotrophin in spontaneous post-stroke recovery remains to be clarified. Besides, while the neuroplastic role of BDNF is restricted to its mature form, most studies investigating the proper effect of ischemia on post-stroke BDNF metabolism focused on mRNA or total protein expressions. In addition, these studies are mainly performed in brain regions collected either at or around the lesion site. Therefore, the objective of the present study was to investigate in both hemispheres, the long-term expression (up to one month) of both pro- and mature BDNF forms in rats subjected to photothrombotic ischemia. These assessments were performed in the cortex and in the hippocampus, two regions known to subserve functional recovery after stroke and were coupled to the study of synaptophysin expression, a marker of synaptogenesis. Our study reports that stroke induces an early and transient increase (4h) in mature BDNF expression in the cortex of both hemispheres that was associated with a delayed rise (30d) in synaptophysin levels ipsilateraly. In both hippocampal territories, the pattern of mature BDNF expression shows a more delayed increase (from 8 to 30d), which coincides with the evolution of synaptophysin expression. Interestingly, in these hippocampal territories, pro-BDNF levels evolve differently suggesting a differential gene regulation between the two hemispheres. While highlighting the complexity of changes in BDNF metabolism after stroke, our data suggest that BDNF involvement in spontaneous post-stroke plasticity is region-dependent. CI - Copyright (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved. FAU - Madinier, A AU - Madinier A AD - Unite INSERM U1093 Cognition, Action et Plasticite Sensorimotrice, Dijon F-21078, France. FAU - Bertrand, N AU - Bertrand N FAU - Rodier, M AU - Rodier M FAU - Quirie, A AU - Quirie A FAU - Mossiat, C AU - Mossiat C FAU - Prigent-Tessier, A AU - Prigent-Tessier A FAU - Marie, C AU - Marie C FAU - Garnier, P AU - Garnier P LA - eng PT - Journal Article DEP - 20121207 PL - United States TA - Neuroscience JT - Neuroscience JID - 7605074 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Synaptophysin) SB - IM MH - Animals MH - Brain/*metabolism/physiopathology MH - Brain Ischemia/*metabolism/physiopathology MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Male MH - Neuronal Plasticity/*physiology MH - Rats MH - Rats, Wistar MH - Stroke/*metabolism/physiopathology MH - Synaptophysin/metabolism MH - Time Factors EDAT- 2012/12/12 06:00 MHDA- 2013/07/26 06:00 CRDT- 2012/12/11 06:00 PHST- 2012/07/24 00:00 [received] PHST- 2012/11/15 00:00 [revised] PHST- 2012/11/28 00:00 [accepted] PHST- 2012/12/11 06:00 [entrez] PHST- 2012/12/12 06:00 [pubmed] PHST- 2013/07/26 06:00 [medline] AID - S0306-4522(12)01165-7 [pii] AID - 10.1016/j.neuroscience.2012.11.054 [doi] PST - ppublish SO - Neuroscience. 2013 Feb 12;231:169-81. doi: 10.1016/j.neuroscience.2012.11.054. Epub 2012 Dec 7.