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大鼠基底前脑内很少有胆碱能神经元共表达甘丙肽信使核糖核酸。

Few cholinergic neurons in the rat basal forebrain coexpress galanin messenger RNA.

作者信息

Miller M A, Kolb P E, Planas B, Raskind M A

机构信息

Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle 98195-6560, USA.

出版信息

J Comp Neurol. 1998 Feb 9;391(2):248-58.

PMID:9518272
Abstract

The concept that galanin (GAL) is cosecreted with acetylcholine (ACh) into the ventral hippocampus is a major component of the current model delineating GAL regulation of the cholinergic memory pathways in the rat. Although GAL-immunoreactivity coexists in 50-70% of cholinergic neurons in the basal forebrain (BF) of colchicine-treated rats, the actual coexistence of these neurotransmitters in the basal state may be lower, because colchicine treatment was recently shown to both induce GAL gene expression and inhibit choline acetyltransferase (ChAT) gene expression in this brain region. We have used single and double in situ hybridization histochemistry to examine the distribution and coexistence of GAL and ChAT mRNAs in the BF of male and female rats. Compared with other forebrain regions, few GAL mRNA-expressing neurons are present within the cholinergic fields of the BF. The greatest number of GAL mRNA-expressing cells in this region are located within the nucleus of the horizontal limb of the diagonal band; but, even in this region, they represent only a small percentage (<20%) of ChAT mRNA-expressing cells. Our results indicate that few cholinergic neurons in the rat BF coexpress GAL mRNA and suggest that, in the basal state, GAL is not widely cosecreted with ACh into hippocampal memory centers.

摘要

甘丙肽(GAL)与乙酰胆碱(ACh)共同分泌到腹侧海马体中的这一概念,是当前描绘GAL对大鼠胆碱能记忆通路调节的模型的主要组成部分。尽管在秋水仙碱处理的大鼠基底前脑(BF)中,50%-70%的胆碱能神经元中存在GAL免疫反应性,但在基础状态下这些神经递质的实际共存情况可能更低,因为最近研究表明秋水仙碱处理既能诱导该脑区的GAL基因表达,又能抑制胆碱乙酰转移酶(ChAT)基因表达。我们使用单重和双重原位杂交组织化学来检测雄性和雌性大鼠BF中GAL和ChAT mRNA的分布及共存情况。与其他前脑区域相比,BF胆碱能区域内表达GAL mRNA的神经元较少。该区域中表达GAL mRNA的细胞数量最多的位于斜角带水平支核内;但是,即使在这个区域,它们也仅占表达ChAT mRNA细胞的一小部分(<20%)。我们的结果表明,大鼠BF中很少有胆碱能神经元共表达GAL mRNA,并提示在基础状态下,GAL不会与ACh广泛共同分泌到海马体记忆中心。

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J Comp Neurol. 1998 Feb 9;391(2):248-58.
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