The nicotinic acetylcholine receptor agonist ABT-594 increases FGF-2 expression in various rat brain regions

被引：26

作者：

Belluardo, N ^{[1
]}

Mudò, G

Caniglia, G

Cheng, QZ

Blum, M

Fuxe, K

机构：

[1] Univ Palermo, Inst Human Physiol, Palermo, Italy

[2] Karolinska Inst, Dept Neurosci, Stockholm, Sweden

[3] Univ Catania, Dept Physiol Sci, I-95125 Catania, Italy

[4] Mt Sinai Sch Med, Fishberg Res Ctr Neurobiol, New York, NY USA

来源：

NEUROREPORT | 1999年 / 10卷 / 18期

关键词：

alpha; 4; beta; 2; subtype; ABT-594; brain; FGF-2; nAChR;

D O I：

10.1097/00001756-199912160-00034

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

THE present experiments were designed to extend previous work showing that acute intermittent (-)nicotine treatment upregulates the level of fibroblast growth factor-2 (FGF2) mRNA in several rat brain regions, by the use of the nicotinic acetylcholine receptor (nAChR) agonist ABT-594 with preferential selectivity for the alpha 4 beta 2 nAChR subtype. ABT594 treatment led to a well-defined temporal and regional upregulation of FGF-2 mRNA. A double labelling analysis showed that the up-regulation of FGF-2 mRNA involves both neuronal and non-neuronal cells. The effects of ABT-594 on FGF-2 expression were antagonized by the preferential alpha 4 beta 2 antagonist dihydro-beta erythroidine (DH beta E), but not by alpha 7 antagonist metyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon alpha 4 beta 2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders. (C) 1999 Lippincott Williams & Wilkins.

引用

页码：3909 / 3913

页数：5

共 24 条

[1] NICOTINE-INDUCED PROTECTION OF CULTURED CORTICAL-NEURONS AGAINST N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED GLUTAMATE CYTOTOXICITY [J].