intervene in MD plasticity by mediating the strengthening of active inputs. The existing information allows envisioning two mechanisms by which ERK could exert its actions on activity-dependent synapse strengthening. First, phosphorylated ERK could, at synaptic level, modulate the activity of substrates important for plasticity such as synaptic proteins ( 22 ), ionic channels ( 23 ), or adhesion molecules (24). A second mode of action involves translocation of phosphorylated ERK to the nucleus

more »

... here it activates, directly or through kinases of the p90 ribosomal S6 kinase family, various transcription factors crucial for plasticity (25, 26).