Autism is a neurodevelopmental disorder in which individuals display a range of challenges in social cognition, language and sensory perception. Sensory perception issues include alterations in visual processing, including reductions in perceptual suppression evident in neuroimaging findings. Such changes in perceptual suppression have recently been shown to relate to reduced action of the inhibitory neurotransmitter GABA in individuals with autism1. This finding, and others in the literature, support the idea that alterations in GABAergic signaling, which cause an imbalance in excitatory/inhibitory neurotransmission, reflect a central characteristic of the neurobiology of autism. This suggests that the GABAergic pathway represents a viable target for drug therapy in autism. Successful development of such drug therapies will require the identification and validation of suitable biomarkers to track neural alterations in GABAergic signaling.
Caroline Robertson aims to test whether alterations in perceptual suppression seen using neuroimaging could serve as a marker of neural response to GABAergic drugs in the brain. Specifically, Robertson proposes to test whether pharmacological augmentation of the GABAergic system can enhance perceptual suppression in healthy control individuals. The ultimate goal of these experiments is to provide a causal and quantifiable link between levels of perceptual suppression and alterations in GABA signaling. Once this biomarker has been established, future studies could utilize perceptual suppression as an index of GABAergic drug efficacy in treatment strategies for individuals with autism.