Mice have been used extensively to model human neurodevelopment disorders (NDDs) and have contributed richly to our understanding of the pathophysiology seen in NDDs. Nevertheless, a key step to realizing the potential of translating findings from pre-clinical models to treatment of human disease is to assess whether cellular and behavioural deficits seen in, for example, mouse models are also present in other rodent models and in addition whether such deficits can also be modelled using human-derived tissue. The ability to generate genetically-modified rats permits extended modelling of NDDs allowing for greater assessment of complex cognitive and social functions and non-invasive imaging. Moreover, as mice and rats last shared a common evolutionary ancestor over 12 million years ago this provides us with an opportunity to test whether the same disease-associated null mutations in these species lead to similar cellular and behavioural deficits. Indeed, although models may have structural validity to human disease, face validity (i.e. models having an equivalent manifestation of a cellular or behavioural outcome) is not necessarily expected given the evolutionary pressures experienced by these two species. Simply put, if mice and rats do not show similar deficits there is little expectation that such models should display face validity with the human condition. Thus, it can be argued that for assessment of NDD models the study of behaviours that rely on brain regions and circuits that are considered to be affected in the human condition is desirable. Furthermore, where robust deficits are present this allows for the assessment of whether pharmacological intervention can ameliorate or reverse dysfunction. In this presentation I will review findings from a large collaborative research programme conducted by colleagues based in the UK and in India that has focussed on cellular and behavioural phenotyping of eight rat models of NDDs. One of these, a model of fragile X syndrome (FXS) which is a major heritable cause of intellectual disability, will be used as an exemplar to illustrate the extent to which some cellular pathophysiologies are conserved in both mouse and rat models but where behavioural deficits are not conserved. In addition, using this rat model of FXS I will present data that indicates that early and brief pharmacological intervention prevents the emergence of a complex associative memory deficit. Furthermore, such early intervention leads to a long-lasting correction of the deficit and is also associated with a rescue of some key cellular pathophysiologies seen in rodent models of FXS. These studies are complemented by experiments with FXS patient induced pluripotent stem cell-derived and isogenic stem cell-derived cortical neurones that reveal altered network excitability and which also highlight the importance of considering both cell autonomous and cell non-autonomous origins of cellular pathophysiology.