Given the importance of spine morphology on synaptic physiology (Nimchinsky et al., 2002; Sala and Segal, 2014; Tønnesen et al., 2014), the increased density and elongation of spines in the fmr1-/y accumbens is likely to contribute to the disrupted synaptic plasticity in the mouse model of Fragile X syndrome. This evidence concerns the gene FMR1 and fragile X syndrome.