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Evidence is mounting that GABA, an inhibitory neurotransmitter, plays a critical role in autism. Genetic studies, animal models, and examination of post-mortem tissue from individuals with autism all suggest the GABA signaling pathway is wired differently in neurotypical and autistic brains. However, studies in living humans to support these claims are sparse, and much has yet to be learned about how exactly GABA may function to give those with autism their unique perspective. One new study from Harvard University and the Massachusetts Institute of Technology helps us understand how people with autism may see the world differently, literally.
Co-authors Drs. Caroline Robertson, Eva-Maria Ratai, and Nancy Kanwisher examined how “binocular rivalry” plays out in the brains of 20 adults with autism and 21 without. Binocular rivalry is the idea that if each of your eyes sees something different, the images will compete with one another for the attention of your brain’s visual processing system. You may perceive one or the other, or a mix of the two images. When you see only one, “perceptual suppression” in the brain is keeping you from perceiving the other.
Figure 1. Example of binocular rivalry when one eye sees the green image and the other the red. From Robertson et al. 2016.
In their new study, Robertson and colleagues showed each participant’s two eyes different images for 45 seconds. The participants pressed different buttons when they saw one image, the other, or a mix. The participants with autism saw a mixture significantly more of the time, demonstrating a reduction in perceptual suppression. This result makes sense in the context of what we know about the potential for individuals with autism to experience “sensory overload.” Participants with autism also switched from one image to the other about half as many times during each trial as the neurotypical participants. Interestingly, participants with autism who exhibited the least perceptual suppression also had the most severe autism-related challenges.
During the trials, the researchers also used magnetic resonance imaging and spectra (MRI and MRS) techniques to measure GABA concentrations in the visual cortex of each participant. In neurotypicals, as GABA concentrations increased in the visual cortex, so did perceptual suppression. However, in participants with autism, there was no relationship between GABA concentration and perceptual suppression, which could indicate that GABA plays a reduced role in binocular rivalry in individuals with autism, or that GABA-related circuitry generates insufficient suppression even when GABA itself is present.
The MRI/MRS also measured glutamate, an excitatory neurotransmitter that acts in opposition to GABA, and several other molecules as controls. Glutamate levels did correlate with perceptual suppression in both neurotypicals and participants with autism. No other molecules the researchers measured correlated with perceptual suppression in either neurotypicals or individuals with autism.
Interestingly, the actual concentration of GABA was not significantly different between neurotypicals and participants with autism. That suggests that it is not simply the presence of GABA that contributes to differences between neurotypicals and autistics, but some difference in the signaling pathway, such as receptors or circuitry. This possibility is consistent with other emerging evidence.
This study provides an important link between a molecular pathway (GABA signaling) and the lived experience of people with autism (altered sensory processing). The authors suggest future work could investigate whether other differences in visual processing can be traced back to differences in GABA signaling. They also recommend tracking GABA signaling at different time points throughout an individual’s development to determine whether altered GABA signaling is a predictor of autism, or arises in response to other neurological changes.
Reference:
Robertson CE, Ratai E & Kanwisher N. (2016). Reduced GABAergic action in the autistic brain. Current Biology, 26:80-85.
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