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Eur J Neurosci ; 25(8): 2425-44, 2007 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-17445239

RESUMO

Previous evidence indicates that locomotor exercise is a powerful means of increasing brain-derived neurotrophic factor (BDNF) and its signal transduction receptor TrkB mRNA levels, immunolabeling intensity and number of BDNF- and TrkB-immunopositive cells in the spinal cord of adult rats but the contribution of specific cell types to changes resulting from long-term activity is unknown. As changes in BDNF protein distribution due to systemic stimuli may reflect either its in-situ synthesis or its translocation from other sources, we investigated where BDNF and TrkB mRNA are expressed in the spinal lumbar segments. We report on the cell types defined by size, BDNF mRNA levels and number of cells with TrkB transcripts in sedentary and exercised animals following 28 days of treadmill walking. In the majority of cells, exercise increased perikaryonal levels of BDNF mRNA but did not affect TrkB transcript levels. Bidirectional changes in a number of TrkB mRNA-expressing cells occurred in small groups of ventral horn neurons. An increase in BDNF transcripts was translated into changes in pro-BDNF and BDNF levels. A 7-day walking regimen increased BDNF protein levels similarly to 28-day treadmill walking. Our observations indicate that long- and short-term locomotor activity of moderate intensity produce stimuli sufficient to recruit a majority of spinal cells to increased BDNF synthesis, suggesting that continuous tuning of pro-BDNF and BDNF levels permits spinal networks to undergo trophic modulation not requiring changes in TrkB mRNA supply.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Locomoção , Condicionamento Físico Animal , Precursores de Proteínas/metabolismo , Receptor trkB/metabolismo , Medula Espinal/metabolismo , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Hibridização In Situ , Vértebras Lombares , Precursores de Proteínas/genética , Distribuição Aleatória , Ratos , Ratos Wistar , Receptor trkB/genética , Medula Espinal/citologia
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