Cognitive function and memory rely on synaptic plasticity - the ability of synapses to modify their strength in response to stimulation. Emerging evidence indicates that post-transcriptional gene regulation is necessary for synaptic plasticity at several levels: by increasing proteome diversity through alternative splicing, or by enabling activity-dependent regulation of mRNA localization, translation or degradation in the dendrite. Mouse knockout studies have linked three RNA-binding proteins, fragile X mental retardation protein, cytoplasmic polyadenylation element binding factor and neuro-oncological ventral antigen to specific aspects of synaptic plasticity. Specificity in the regulation of synaptic plasticity might, in part, relate to the functional coherence of proteins encoded by the RNA targets of each RNA-binding protein.