Disruption of normal brain development during pregnancy and in infancy can lead to life-long neurological disorders. As the brain develops, there is increasing complexity of cellular structure, connectivity and functional activity. This pattern is essential for normal brain development and disruption to these early developmental processes leads to long-term dysfunction, including neurodevelopmental disorders such as epilepsy, and autismspectrum disorder (ASD). Recent work from our lab has shown that alteration in GABAergic signaling, using Muscimol, during early neuronal development in vitro alters the morphological and physiological development of neurons, creating networks that appear to be less complex but hyperexcitable. In vivo, a similar pharmacological intervention results in early changes in brain structure, and behavioural differences in adults that suggest social deficits or depressive-like behaviour. However, the structural connectivity of the brain that links brain volume changes with behavioural deficits are yet to be determined. The specific aim of this study is to determine the deficits in neuronal morphology that underly brain injury produced by developmental exposure to a GABAA receptor agonist. As part of this, dendritic arborization, dendritic spine number and the number of chemically mature synapses will be assessed. The successful candidate will join the Neurodevelopmental Injury lab, based at the RVC Camden campus, and gain expertise in primary culture, live and fixed cell microscopy, immunohistochemistry, protein and RNA analyses. Outcomes: This work will provide an important link between cellular complexity during development and behavioural differences detected in adulthood. The specific structural changes that occur, and the time and sexdependence of these changes, have important implications in the treatment of neurodevelopmental disorders.