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运动锻炼会改变成年大鼠脊髓中前脑源性神经营养因子、脑源性神经营养因子及其受体TrkB的表达。

Locomotor exercise alters expression of pro-brain-derived neurotrophic factor, brain-derived neurotrophic factor and its receptor TrkB in the spinal cord of adult rats.

作者信息

Macias Matylda, Dwornik Anna, Ziemlinska Ewelina, Fehr Susanna, Schachner Melitta, Czarkowska-Bauch Julita, Skup Malgorzata

机构信息

Department of Neurophysiology, Nencki Institute of Experimental Biology, 3 Pasteur Street, 02-093 Warsaw, Poland.

出版信息

Eur J Neurosci. 2007 Apr;25(8):2425-44. doi: 10.1111/j.1460-9568.2007.05498.x.

DOI:10.1111/j.1460-9568.2007.05498.x
PMID:17445239
Abstract

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.

摘要

先前的证据表明,运动锻炼是提高成年大鼠脊髓中脑源性神经营养因子(BDNF)及其信号转导受体TrkB mRNA水平、免疫标记强度以及BDNF和TrkB免疫阳性细胞数量的有效手段,但长期活动所导致的变化中特定细胞类型的作用尚不清楚。由于全身刺激引起的BDNF蛋白分布变化可能反映其原位合成或从其他来源的转运,我们研究了BDNF和TrkB mRNA在脊髓腰段的表达位置。我们报告了在跑步机上行走28天后,久坐不动和运动的动物中根据大小、BDNF mRNA水平和具有TrkB转录本的细胞数量所定义的细胞类型。在大多数细胞中,运动增加了BDNF mRNA的核周水平,但不影响TrkB转录本水平。在一小群腹角神经元中,表达TrkB mRNA的细胞数量出现了双向变化。BDNF转录本的增加转化为前体BDNF和BDNF水平的变化。7天的行走方案与28天的跑步机行走一样增加了BDNF蛋白水平。我们的观察结果表明,中等强度的长期和短期运动活动产生的刺激足以促使大多数脊髓细胞增加BDNF合成,这表明前体BDNF和BDNF水平的持续调节使脊髓网络能够进行营养调节,而无需改变TrkB mRNA的供应。

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