Central nicotinic receptors, neurotrophic factors and neuroprotection

Natale Belluardo, Giuseppa Mudò, Mariann Blum, Kjell Fuxe

Research output: Contribution to journalArticlepeer-review

163 Scopus citations


The multiple combinations of nAChR subunits identified in central nervous structures posses distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely indicate a neuroprotective/trophic role of nAChR activation involving mainly α7 and α4β2 nAChR subtypes, as evidenced using selective nAChR antagonists, and by potent nAChR agonists recently found displaying efficacy and/or larger selective affinities than (- )-nicotine for neuronal nAChR subtypes. A neurotrophic factor gene regulation by nAChR signalling has been taken into consideration as possible mechanism involved in neuroprotective/trophic effects by nAChR activation and has evidenced an involvement of the fibroblast growth factor (FGF-2) gene as a target of nAChR signalling. These findings suggested that FGF-2 could be involved, according to the FGF-2 neurotrophic functions, in nAChR mechanisms mediating the neuronal survival, trophism and plasticity. (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)21-34
Number of pages14
JournalBehavioural Brain Research
Issue number1-2
StatePublished - Aug 2000
Externally publishedYes


  • FGF-2
  • nAChR
  • Neuroprotection
  • Neurotrophic factors

ASJC Scopus subject areas

  • Behavioral Neuroscience


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