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衰老大鼠海马结构中脑源性神经营养因子(BDNF)和酪氨酸激酶受体B(trkB)mRNA的表达

BDNF and trkB mRNA expression in the hippocampal formation of aging rats.

作者信息

Lapchak P A, Araujo D M, Beck K D, Finch C E, Johnson S A, Hefti F

机构信息

Division of Neurogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191.

出版信息

Neurobiol Aging. 1993 Mar-Apr;14(2):121-6. doi: 10.1016/0197-4580(93)90087-r.

DOI:10.1016/0197-4580(93)90087-r
PMID:8487914
Abstract

Quantitative in situ hybridization and northern blot analysis techniques were used to determine the topographical distribution and levels of mRNA coding for brain-derived neurotrophic factor (BDNF) and the tyrosine receptor kinase (trkB) mRNA in the hippocampal formation of two strains of male rat during aging. Age did not change the prevalence or regional distribution patterns of BDNF or trkB mRNA in the hippocampal formation throughout the lifespan of male Sprague-Dawley rats. There also were no significant differences in the prevalence or topographical distribution patterns of trkB mRNA transcripts during aging. Northern blot analysis of hippocampal RNA from male Fischer 344 confirmed that neither BDNF mRNA nor trkB mRNA levels changed with age. These findings suggest that age-related neurodegenerative changes, including the atrophy of the cholinergic septo-hippocampal pathway, are not the result of changes in hippocampal BDNF or trkB mRNA expression. Moreover, the prevalence and distribution of synaptosomal-associated protein 25 (SNAP-25), a neuron-specific protein located in synaptic terminals and a putative marker of synaptic integrity, did not change with age. These findings indicate that altered hippocampal synaptic plasticity which occurs in the aged rat brain is not a reflection of changes in the expression of BDNF or trkB receptor mRNA.

摘要

采用定量原位杂交和Northern印迹分析技术,以确定衰老过程中两种雄性大鼠品系海马结构中脑源性神经营养因子(BDNF)编码mRNA和酪氨酸受体激酶(trkB)mRNA的拓扑分布及水平。在雄性Sprague-Dawley大鼠的整个寿命期内,年龄并未改变海马结构中BDNF或trkB mRNA的患病率或区域分布模式。衰老过程中trkB mRNA转录本的患病率或拓扑分布模式也无显著差异。对雄性Fischer 344大鼠海马RNA进行的Northern印迹分析证实,BDNF mRNA和trkB mRNA水平均未随年龄变化。这些发现表明,与年龄相关的神经退行性变化,包括胆碱能隔海马通路的萎缩,并非海马BDNF或trkB mRNA表达变化的结果。此外,位于突触终末的神经元特异性蛋白、突触完整性的假定标志物——突触体相关蛋白25(SNAP-25)的患病率和分布也未随年龄改变。这些发现表明,老年大鼠脑中发生的海马突触可塑性改变并非BDNF或trkB受体mRNA表达变化的反映。

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