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Neuroprotective effect of exercise in rat hippocampal slices submitted to in vitro ischemia is promoted by decrease of glutamate release and pro‐apoptotic markers
Author(s) -
Mourão Flávio Afonso Gonçalves,
Leite Hércules Ribeiro,
Carvalho Luciana Estefani Drumond,
Ferreira e Vieira Talita Hélen,
Pinto Mauro Cunha Xavier,
Castro Medeiros Daniel,
Andrade Ian Lara Lamounier,
Gonçalves Daniela Fontes,
Pereira Grace Schenatto,
Dutra Moraes Márcio Flávio,
Massensini André Ricardo
Publication year - 2014
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.12786
Subject(s) - neuroprotection , excitotoxicity , glutamate receptor , hippocampal formation , apoptosis , ischemia , glutamatergic , neuroscience , pharmacology , programmed cell death , biology , medicine , biochemistry , receptor
The role of physical exercise as a neuroprotective agent against ischemic injury has been extensively discussed. Nevertheless, the mechanisms underlying the effects of physical exercise on cerebral ischemia remain poorly understood. Here, we investigate the hypothesis that physical exercise increases ischemic tolerance by decreasing the induction of cellular apoptosis and glutamate release. Rats ( n = 50) were submitted to a swimming exercise protocol for 8 weeks. Hippocampal slices were then submitted to oxygen and glucose deprivation. Cellular viability, pro‐apoptotic markers (Caspase 8, Caspase 9, Caspase 3, and apoptosis‐inducing factor), and glutamate release were analyzed. The percentage of cell death, the amount of glutamate release, and the expression of the apoptotic markers were all decreased in the exercise group when compared to the sedentary group after oxygen and glucose deprivation. Our results suggest that physical exercise protects hippocampal slices from the effects of oxygen and glucose deprivation, probably by a mechanism involving both the decrease of glutamatergic excitotoxicity and apoptosis induction.Exercise reduces excitotoxicity and apoptosis. The mechanisms underlying neuroprotective effects of regular exercise are still not fully understood. Here, we showed that swim training promotes neuroprotection decreasing pro‐apoptotic markers as caspases 8, 9, 3, and apoptose‐Inducing Factor (AIF) as well as glutamate release from hippocampal slices. Our data reinforce the idea that exercise affords a neuroprotective effect.