Fragile X Syndrome (FXS) is the most common inherited form of intellectual disability. It is characterised by developmental delay and cognitive impairment and many affected individuals have autistic-like behaviours. The predominant cause of FXS is the transcriptional silencing of the fragile X mental retardation gene (FMR1) and loss of the corresponding protein (FMRP). The cognitive and behavioural features of FXS first emerge over the first two years of life, correlating well with the rapid phase of synaptogenesis in the cerebral cortex. In mouse models of FXS the critical period for the maturation of glutamate receptor signalling at thalamocortical synapses is delayed (1) and there is an increase in dendritic filopodia in layer IV of the primary somatosensory cortex (S1). We hypothesized that genetic deletion of Fmr1 in mice (2) causes a general delay in synaptogenesis. To test this hypothesis, we compared the morphological features of synapses in layers II-III and IV of S1 at P14 and P35 by electron microscopy (3). No differences were detected between genotypes (Fmr1-/y [P14: N=7, P35: N=5] and Fmr1+/y [P14: N=8, P35 N=4]) in synaptic density, PSD length, number of presynaptic vesicles/µm of PSD or number of docked vesicles/µm of PSD at either age. Furthermore, age-dependent changes in these parameters were not significantly different in the Fmr1-/y mice compared to controls indicating a similar time-course of synaptic maturation. We next examined mRNA levels in S1 for a selection of synaptic proteins at P7 and P14 [N=5 per genotype and age] using qPCR (3). Again, no differences were detected between Fmr1-/y and Fmr1+/y at either age or in the magnitude of the age-dependent changes in expression. This study suggests that the loss of FMRP does not cause a general developmental delay of synaptogenesis in primary somatosensory cortex in a mouse model of FXS.