2024-03-29T09:16:59Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/458142022-11-17T02:08:08Zhdl_2115_20040hdl_2115_121Gene and protein analysis of brain derived neurotrophic factor expression in relation to neurological recovery induced by an enriched environment in a rat stroke modelHirata, KenjiKuge, YujiYokota, ChiakiHarada, AkinaKokame, KoichiInoue, HiroyasuKawashima, HidekazuHanzawa, HirokoShono, YujiSaji, HideoMinematsu, KazuoTamaki, NagaraFocal ischemiaEnriched environmentBrain derived neurotrophic factor491Although an enriched environment enhances functional recovery after ischemic stroke, the mechanism underlying this effect remains unclear. We previously reported that brain derived neurotrophic factor (BDNF) gene expression decreased in rats housed in an enriched environment for 4 weeks compared to those housed in a standard cage for the same period. To further clarify the relationship between the decrease in BDNF and functional recovery, we investigated the effects of differential 2-week housing conditions on the mRNA of BDNF and protein levels of proBDNF and mature BDNF (matBDNF). After transient occlusion of the right middle cerebral artery of male Sprague-Dawley rats, we divided the rats into two groups: (1) an enriched group housed multiply in large cages equipped with toys, and (2) a standard group housed alone in small cages without toys. Behavioral tests before and after 2-week differential housing showed better neurological recovery in the enriched group than in the standard group. Synaptophysin immunostaining demonstrated that the density of synapses in the peri-infarct area was increased in the enriched group compared to the standard group, while infarct volumes were not significantly different. Real-time reverse transcription polymerase chain reaction, Western blotting and immunostaining all revealed no significant difference between the groups. The present results suggest that functional recovery cannot be ascribed to an increase in matBDNF or a decrease in proBDNF but rather to other underlying mechanisms.Elsevier IrelandJournal Articleapplication/pdfhttp://hdl.handle.net/2115/45814https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/45814/1/NL495-3_210-215.pdf0304-3940Neuroscience Letters49532102152011-05-20enginfo:pmid/21457756info:doi/10.1016/j.neulet.2011.03.068author