Autism Spectrum Disorder (ASD) and related Neurodevelopmental Disorders such as ADHD are clinically diverse, and their etiological mechanisms are poorly understood. This makes finding treatments challenging. What is needed is a better understanding of causal pathways to identify sub-groups and inform the search for personalised prevention and treatment strategies. There is fresh hope however, based on preclinical, genomic and post-mortem evidence that multiple risk factors for ASD converge to disrupt the balance between excitatory glutamate (E) and inhibitory GABA (I) in brain. This is postulated to disrupt the activity and microstructure of developing brain circuits. We are testing this hypothesis by examining the link between risk factors for ASD and spontaneous functional activity and microstructure in the fetal, neonatal and infant brain in individuals with and without a family history of ASD. We also want to know whether E/I abnormalities persist into adulthood in ASD, and if they are ‘responsive’ to pharmacological modulation.