Nicotine-induced FGF-2 mRNA in rat brain is preserved during aging
Nicotine-induced FGF-2 mRNA in rat brain is preserved during aging
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DOI：
10.1016/j.neurobiolaging.2004.01.002
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发表时间：
2004-11-01
影响因子：
4.2
通讯作者：
Fuxe, K
中科院分区：
文献类型：
--
作者：
Belluardo, N;Mudò, G;Fuxe, K
根据描述尼古丁作为认知增强剂、提高警惕性和改善学习和记忆的观察结果，表明尼古丁在衰老过程中对大脑的间接营养作用，体外和体内模型均证明了nAChR激动剂的神经保护作用。以前，我们已经报道了急性间歇性（-）尼古丁治疗显着增加成纤维细胞生长因子-2（FGF-2）的mRNA和蛋白质在几个大脑区域的大鼠大脑。本研究旨在分析尼古丁诱导的FGF-2在大鼠大脑中的表达是否在衰老过程中得以保留。采用原位杂交和定量RNase保护试验，本文报道了在衰老过程中（12和24月龄大鼠），大鼠脑中FGF-2基因表达对（-）尼古丁刺激nAChR的反应是完全有效的，涉及神经元和胶质细胞。这项研究扩展到FGF家族的其他成员，如FGF-5和-20，但在研究的任何年龄，这种表达都不受（-）尼古丁治疗的影响。同样，在（-）尼古丁处理后，在成年和老年大鼠中未观察到FGF受体（FGFR 1-3）mRNA水平的变化。综上所述，目前和以前的数据支持以下假设：（-）尼古丁的神经保护作用和（-）尼古丁激动剂在治疗阿尔茨海默病和帕金森病中的潜在有益作用可能至少部分涉及神经元和神经胶质FGF-2信号传导的激活。分析nAChR激活与FGF-2上调之间联系的机制的工作正在进行中。(C)2004年爱思唯尔公司All rights reserved.
Indirect trophic actions of nicotine on brain during aging are suggested from observations describing nicotine as a cognitive enhancer, increasing vigilance and improving learning and memory, and both in vitro and in vivo models have demonstrated neuroprotective effects of nAChR agonists. Previously, we have reported that an acute intermittent (-)nicotine treatment significantly increases fibroblast growth factor-2 (FGF-2) mRNA and protein in several brain regions of rat brain. The present study was designed to analyse if nicotine-induced FGF-2 expression in the rat brain was preserved during aging. Using in situ hybridization and quantitative RNase protection assay the present paper reports that during aging (12- and 24-month-old rats) the response of FGF-2 gene expression in the rat brain to nAChR stimulation by (-)nicotine is fully effective and involves both neurons and glial cells. The investigation was extended to other members of the FGF family, such as FGF-5 and -20, but this expression was not influenced by the (-)nicotine treatment at any age studied. Similarly following (-)nicotine treatment no changes were observed in FGF receptors (FGFR 1-3) mRNA levels in adult and aged rats. Taken together, the present and previous data support the hypothesis that neuroprotective effects of (-)nicotine and the potential beneficial effects of (-)nicotine agonists in the treatment of Alzheimer's and Parkinson's diseases, may at least in part involve an activation of the neuronal and glial FGF-2 signalling. Work is in progress to analyse the mechanism(s) linking nAChR activation to the up-regulation of FGF-2. (C) 2004 Elsevier Inc. All rights reserved.