Long-term effects of environmental stimulation following hypoxia-ischemia on the oxidative state and BDNF levels in rat hippocampus and frontal cortex.
Environmental enrichment recovers memory deficits without affecting atrophy of the hippocampus adult rats submitted to neonatal hypoxia-ischemia (HI). The present study was designed to investigate whether the modulation of brain oxidative status and/or BDNF content, as assessed in adulthood, are involved with the functional neuroprotection caused by environmental enrichment in animals receiving neonatal HI. Male Wistar rats, in the 7th postnatal day, were submitted to the Levine-Rice model of neonatal hypoxia-ischemia, comprising permanent occlusion of the right common carotid artery and a 90 min period of hypoxia (8% O(2)-92% N(2)). Starting 2 weeks after the HI event, animals were stimulated by the enriched environment (1 h/day for 9 weeks). Rats were sacrificed approximately 24 h after the end of enrichment period and some oxidative stress parameters, specifically the free radical levels, macromolecules damage and superoxide dismutase activity, in hippocampus and frontal cortex samples were determined. BDNF levels were also measured in the same encephalic structures. Indexes of macromolecules damage, TBARS levels and total cellular thiols, as well as free radical levels were unchanged in both studied structures. An increased SOD activity in the right hippocampus of HI group maintained in standard environment was found, this effect was reversed in HI enriched group. Moreover, BDNF levels were increased only in the hippocampus of non-stimulated HI group. These results suggest that the environmental enrichment protocol bearing cognitive protection is not associated to increases in BDNF expression nor SOD activity in hippocampus of the rats, as assessed in adulthood, submitted to neonatal hypoxia-ischemia.
Pereira
Lenir Orlandi
LO
Programa de Pós Graduação em Ciências Biológicas-Neurociências, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500 sala 107, 90050- 170, Porto Alegre, RS, Brazil. lenir_pereira@yahoo.com.br
Nabinger
Patrícia Machado
PM
Strapasson
Atahualpa Cauê Paim
AC
Nardin
Patrícia
P
Gonçalves
Carlos Alberto Saraiva
CA
Siqueira
Ionara Rodrigues
IR
Netto
Carlos Alexandre
CA
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D019610:Cytoprotection / Q000502:physiology*; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D004777:Environment; D005609:Free Radicals / Q000378:metabolism; D005625:Frontal Lobe / Q000378:metabolism / Q000503:physiopathology; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013995:Time
D019208:Brain-Derived Neurotrophic Factor; D005609:Free Radicals; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1