Nicotine-induced FGF-2 mRNA in rat brain is preserved during aging.

Indirect trophic actions of nicotine on brain during aging are suggested from observations describing nicotine as a cognitive enhancer, increasing vigilance and improving learning and memory, and both in vitro and in vivo models have demonstrated neuroprotective effects of nAChR agonists. Previously, we have reported that an acute intermittent (-)nicotine treatment significantly increases fibroblast growth factor-2 (FGF-2) mRNA and protein in several brain regions of rat brain. The present study was designed to analyse if nicotine-induced FGF-2 expression in the rat brain was preserved during aging. Using in situ hybridization and quantitative RNase protection assay the present paper reports that during aging (12- and 24-month-old rats) the response of FGF-2 gene expression in the rat brain to nAChR stimulation by (-)nicotine is fully effective and involves both neurons and glial cells. The investigation was extended to other members of the FGF family, such as FGF-5 and -20, but this expression was not influenced by the (-)nicotine treatment at any age studied. Similarly following (-)nicotine treatment no changes were observed in FGF receptors (FGFR 1-3) mRNA levels in adult and aged rats. Taken together, the present and previous data support the hypothesis that neuroprotective effects of (-)nicotine and the potential beneficial effects of (-)nicotine agonists in the treatment of Alzheimer's and Parkinson's diseases, may at least in part involve an activation of the neuronal and glial FGF-2 signalling. Work is in progress to analyse the mechanism(s) linking nAChR activation to the up-regulation of FGF-2.