The function of brain circuits relies on high-fidelity information transfer, precisely controlling integration of synaptic input, leading to neuronal output. Synaptic inputs arrive primarily at dendrites, where they undergo integration and summation throughout the somatodendritic domain, ultimately leading to axonal output. Emerging evidence suggests that the ability of neurons to transfer synaptic information and modulate their output is impaired in the neurodevelopmental disorder Fragile X Syndrome. Indeed, how neurons may or may not respond to sensory information during development that leads to compensation of their activity appears to be a salient feature of rodent models of Fragile X Syndrome. In this review we summarise recent findings that have shone light on the ability of neurons in sensory and limbic circuits to reliably code information. We highlight which aspects of this transform are underlain by either direct loss of FMRP in Fragile X Syndrome and which likely result from compensatory or homeostatic alterations to neuron function. Dissection of these mechanisms effect on neuronal plasticity throughout development will have direct implications for individuals with Fragile X Syndrome, directing the timing and duration of different treatment options.