ABSTRACT The prefrontal cortex and amygdala are strongly and consistently implicated in most behaviorally-defined neurodevelopmental disorders, including the autism (ASD) and psychosis spectrum disorders, such as schizophrenia (SCZ). Although ASD and SCZ do differ in some core symptomatology, they share common neurobiological, genetic, and behavioral features – chiefly socioemotional impairments and anxiety. We hypothesize that the medial prefrontal cortex (mPFC) and amygdala, key neural circuitry that regulates anxiety, will show similar neuropathological features across the disorders, specifically reduced inhibitory control over the circuit via the GABAergic system that would normally keep anxiety in check. Widespread evidence in other brain regions, including the dorsolateral prefrontal cortex (dlPFC), point to either reductions in the number of GABAergic interneurons and/or transmission of GABA in ASD and SCZ. However, GABAergic control via the mPFC-amygdala pathway that modulates anxiety has surprisingly not been examined in either disorder. This key gap in knowledge hinders development of targeted, neuroscience-driven biotherapeutics. We propose to take the fundamental first step to determine if alterations in the GABAergic system of mPFC supra- and infra- granular layers (Specific Aim 1) and amygdala total, lateral, basal, accessory basal, and central nuclei (Specific Aim 2) in the brains of individuals with ASD and/or SCZ relative to age- and sex-matched control brains are due to a: i) decrease in the number of GABAergic cells – defined by presence of glutamate decarboxylase-67—GAD67 (i.e. GAD1), the enzyme required for GABA synthesis, and/or ii) decrease in GABA production from interneurons to pyramidal/principal excitatory neurons – measured by GAD67 mRNA transcription levels. In addition, we hypothesize that a subclass of GABAergic inhibitory neurons that are parvalbumin positive (PV+) will disproportionately be reduced in mPFC infragranular layers as well as amygdala lateral and basal nuclei. Lastly, given findings from our previous work, we anticipate age-related changes in these regions and therefore will limit this study to 36 well-characterized age- and sex-matched adult brains from our collection. Our findings will serve as a fundamental reference for which mechanistic studies and animal models of these uniquely human disorders can be built upon.