Acetylcholine, acting on both nicotinic receptors (nAChRs) and muscarinic receptors (mAChRs), plays a role
in the regulation of synaptic plasticity, being involved in the regulation of cellular processes and cognitive functions, such
as learning, memory and attention. Recently, G protein coupled receptors (GPCRs), including mAChRs, have been reported
to transactivate tyrosine-kinase receptors (RTK), such as epidermal growth factor receptor (EGFR), and initiate
their intracellular signaling. In this minireview we have first analysed the RTK transactivation mechanisms, involving
cholinergic receptors, and thereafter the interplay between AChR and neurotrophic factor systems built up by FGF2 and
fibroblast growth factor receptor 1 (FGFR1). Although mAChR and FGFR1 activate common signaling pathways, playing
similar roles in the regulation of central nervous system (CNS) plasticity and trophism, this analysis revealed that at the
present there are no data reporting an involvement of cholinergic receptors in the FGFR1 transactivation. However, here
we reported preliminary results on FGFR1 transactivation by mAChRs, suggesting a possible interaction between mAChR
and neurotrophic factor receptors, with potential relevance for cognitive functions.
Keywords: FGFR1, G protein coupled receptor, Muscarinic receptors, Nicotinic receptors, Receptor-receptor interaction, Synaptic
plasticity, Transactivation, Tyrosine-kinase receptors.
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