Five to 30% of individuals with autism spectrum disorders (ASD) have co-morbid epilepsy, and a common mechanistic link may exist. The underlying pathophysiology of this co-morbidity remains unknown. Evidence suggests that a single inflammatory event during the perinatal period can lead to ASD-like behaviours and there is growing evidence to support the contribution of inflammation to the development of epilepsy. The aim of the work presented in this thesis is to develop, validate, and use a co-morbid mouse model to investigate the common mechanism(s) involved in the pathogenesis of ASD and epilepsy and possible treatment options. We found that a postnatal immune challenge reduced the seizure threshold in a mouse model of ASD (BTBR T+Itpr3tf/J mice), as well as induced spontaneous and unprovoked electrographic seizure activity. We validated co-morbid epilepsy in this mouse model of ASD by optimizing a system to telemetrically record video-EEG in a mouse for a continuous 4-week period. We did not find any changes in the ASD-like behaviours of the adult BTBR mice postnatally treated with LPS compared to controls and no change in the hippocampal cytokine levels that were measured. The co-morbid mouse model was used to pharmacologically target mechanisms that regulate inhibitory tone and quantify the observed behavioural changes. We observed an increase in seizure threshold when mice were pre-treated with bumetanide and found that there were alterations in GABA-induced behaviours such as delayed loss of righting reflex and onset of sedation after diazepam administration in adult BTBR mice. These findings suggest that underlying disruptions in chloride homeostasis and function of the GABAergic system may be a major contributory mechanism to the pathogenesis of ASD and epilepsy. Lastly, we found that the ketogenic diet had a protective effect against postnatal immune challenge-induced seizure threshold decreases and the reversal of delay in diazepam-induced behaviours. Our findings provide support that the anti-seizure effects of KD may be due to a iii restoration of inhibitory tone. A better understanding of the mechanisms that contribute to the comorbid development of ASD and epilepsy will facilitate optimization of treatment options and improve quality of life for individuals with this co-morbidity.