6533b836fe1ef96bd12a1605

RESEARCH PRODUCT

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

Qingzhang ChengGiuseppa MudòGiuseppa CanigliaKjell FuxeNatale BelluardoMariann Blum

subject

Agonistmedicine.medical_specialtyPyridinesmedicine.drug_classBiologyRats Sprague-DawleyNicotinechemistry.chemical_compoundDownregulation and upregulationInternal medicinemedicineAnimalsTissue DistributionNicotinic AgonistsRNA MessengerIn Situ HybridizationAcetylcholine receptorNeuronsMethyllycaconitineGeneral NeuroscienceAntagonistBrainDihydro-beta-ErythroidineImmunohistochemistryRatsNicotinic acetylcholine receptorNicotinic agonistEndocrinologynervous systemchemistryAzetidinesFibroblast Growth Factor 2medicine.drug

description

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 alpha4beta2 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 alpha4beta2 antagonist dihydrobetaerythroidine (DHbetaE), but not by alpha7 antagonist methyllycaconitine (MLA). In conclusion, FGF-2 mRNA levels can be increased in several brain regions upon alpha4beta2 nAChR activation, suggesting a therapeutic significance in neurodegenerative disorders.

yearjournalcountryeditionlanguage
2000-03-15
http://www.scopus.com/inward/record.url?eid=2-s2.0-0033576771&partnerID=MN8TOARS