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

Natale Belluardo; Giuseppa Mudò; Giuseppa Caniglia; Qingzhang Cheng; Mariann Blum; Kjell Fuxe

doi:10.1097/00001756-199912160-00034

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

Natale Belluardo, Giuseppa Mudò, Giuseppa Caniglia, Qingzhang Cheng, Mariann Blum, Kjell Fuxe

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

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 α4β2 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 α4β2 antagonist dihydro-βerythroidine (DHβE), but not by α7 antagonist metyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon α4β2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders.

Original language	English (US)
Pages (from-to)	3909-3913
Number of pages	5
Journal	NeuroReport
Volume	10
Issue number	18
DOIs	https://doi.org/10.1097/00001756-199912160-00034
State	Published - Dec 16 1999
Externally published	Yes

Keywords

ABT-594
Brain
FGF-2
NAChR
α4β2 subtype

ASJC Scopus subject areas

Neuroscience(all)

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10.1097/00001756-199912160-00034

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

abstract = "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 α4β2 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 α4β2 antagonist dihydro-βerythroidine (DHβE), but not by α7 antagonist metyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon α4β2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders.",

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author = "Natale Belluardo and Giuseppa Mud{\`o} and Giuseppa Caniglia and Qingzhang Cheng and Mariann Blum and Kjell Fuxe",

year = "1999",

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doi = "10.1097/00001756-199912160-00034",

language = "English (US)",

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AU - Belluardo, Natale

AU - Mudò, Giuseppa

AU - Caniglia, Giuseppa

AU - Cheng, Qingzhang

AU - Blum, Mariann

AU - Fuxe, Kjell

PY - 1999/12/16

Y1 - 1999/12/16

N2 - 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 α4β2 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 α4β2 antagonist dihydro-βerythroidine (DHβE), but not by α7 antagonist metyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon α4β2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders.

AB - 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 α4β2 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 α4β2 antagonist dihydro-βerythroidine (DHβE), but not by α7 antagonist metyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon α4β2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders.

KW - ABT-594

KW - Brain

KW - FGF-2

KW - NAChR

KW - α4β2 subtype

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

Abstract

Keywords

ASJC Scopus subject areas

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