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 up-regulation 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.