title: Postischemic exercise attenuates whereas enriched environment has certain enhancing effects on lesion-induced subventricular zone activation in the adult rat.
abstract: Experimental stroke increases cell proliferation and neurogenesis in the subventricular zone (SVZ) and in the dentate gyrus subgranular zone (SGZ) in the adult mammalian brain. This study examined the effects of postischemic voluntary exercise (running wheel) and environmental enrichment on the SVZ and SGZ 1 week after focal cortical ischemia in adult spontaneously hypertensive rats. Immunohistochemical labeling was performed for incorporation of specific cell markers such as Ki67 and 5-bromodeoxyuridine (proliferating and newborn cells), terminal deoxynucleotidyl transferase-mediated dUTP in situ nick-end labeling (apoptotic cells), Sox-2 and glial fibrillary acidic protein (neural stem and progenitor cells), polysialylated neural cell adhesion molecule and doublecortin (neuroblasts). Postischemic exercise and environmental enrichment differentially modulated SVZ cell genesis but lacked effects on the SGZ. Lesion-induced proliferation of neural stem/progenitor cells and neuronal precursors was attenuated in stroke runners without any effects on apoptosis or neuronal migration in the forebrain. Running activity did not affect the SVZ in intact rats. In contrast to postischemic wheel running, postischemic environmental enrichment did not have attenuating effects on the ipsilateral SVZ and increased proliferating putative neural stem cells and neuronal precursors contralaterally. A significant functional improvement, assessed using a rotating pole, was observed only in the postischemically enriched group and was likely due to other types of plasticity than neuronal replacement at this early time point. It may be concluded that in contrast to enriched environment, exercise during the first postischemic week might be detrimental for regenerative processes initiated in the SVZ after stroke.
authors.affiliation: The Arvid Carlsson Institute at the Institute of Clinical Neuroscience, Medicinaregatan 11, Box 432, 405 30 Göteborg, Sweden. mila.komitova@neuro.gu.se
authors.forename: Mila
authors.initials: M
authors.lastname: Komitova
authors.forename: Li Ru
authors.initials: LR
authors.lastname: Zhao
authors.forename: Gunilla
authors.initials: G
authors.lastname: Gidö
authors.forename: Barbro B
authors.initials: BB
authors.lastname: Johansson
authors.forename: Peter
authors.initials: P
authors.lastname: Eriksson
mesh_terms: D000367:Age Factors; D000818:Animals; D000963:Antimetabolites; D017209:Apoptosis; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D001973:Bromodeoxyuridine; D002455:Cell Division; D018891:Dentate Gyrus / Q000473:pathology / Q000502:physiology; D000089662:Doublecortin Protein; D004780:Environment, Controlled; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D009043:Motor Activity; D009416:Nerve Regeneration; D009474:Neurons / Q000166:cytology; D005082:Physical Exertion; D051381:Rats; D011918:Rats, Inbred SHR; D013234:Stem Cells / Q000166:cytology
chemical_list: D000963:Antimetabolites; C000714848:Dcx protein, rat; D000089662:Doublecortin Protein; D001973:Bromodeoxyuridine