Neurotrophic effects of central nicotinic receptor activation

N. Belluardo, G. Mudo, M. Blum, G. Amato, K. Fuxe

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

A growing number of data have shown that compounds interacting with neuronal nicotinic acetylcholine receptors (nAChRs) have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improvement 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 disease and Parkinson's disease. This neuroprotective/trophic role of nAChR activation has been mainly mediated by 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 a possible mechanism involved in neuroprotective/trophic effects of nAChR activation and has given evidence that the fibroblast growth factor (FGF-2) gene is a target for nAChR signalling. These findings suggested that FGF-2 could be involved, in view of its neurotrophic functions, in nAChR mechanisms mediating neuronal survival, trophism and plasticity.

Original languageEnglish (US)
Pages (from-to)227-245
Number of pages19
JournalJournal of Neural Transmission, Supplement
Volume60
DOIs
StatePublished - 2000
Externally publishedYes

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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