GABAergic Action Found to Play a Central Role in Autism

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Disturbances in the GABAergic signaling pathway may be the cause of the dysfunction in GABAergic activity.
Disturbances in the GABAergic signaling pathway may be the cause of the dysfunction in GABAergic activity.

A basic inability to selectively suppress optical signals may be a significant mechanism in the expression of autism, according to research published in the January issue of Current Biology.1

In normal individuals, visual information is selected from separate, simultaneous images presented to each of the two eyes via a process called binocular rivalry, in which the less dominant image is suppressed over many seconds. The study revealed a “robust, replicated autistic deficit” in binocular rivalry that was attributed to an imbalance in the interplay of excitation and inhibition occurring in the visual cortex of the brain.

Through examination of the dynamics of binocular rivalry in 41 individuals (21 of whom were diagnosed with autism and 20 normal controls), Caroline Robertson, PhD, from Harvard University and MIT's McGovern Institute for Brain Research and colleagues found both a slower rate of binocular switching and reduced periods of perceptual suppression among autistic individuals that directly correlated with clinical measures, supporting previous evidence of disruptions in binocular rivalry as a marker for autism.2

The strength of perceptual suppression is believed to hinge on the right balance of inhibitory/excitability signal mediation.3 Reduced levels of the neurotransmitter, ¥-aminobutyric acid (GABA), correlate with reduced inhibitory action, while reductions in glutamate are associated with interference in the recurrent excitation necessary to achieve strong perceptual dominance.2,3 To identify which of these neurotransmitters was most significant to impairment of binocular rivalry in autism, both were measured via magnetic resonance spectroscopy (MRS). Although glutamate and GABA concentrations both appeared consistent between the autistic group and the normal controls, the action of glutamate was conserved in autism, while the action of GABA was impaired.

The investigators found that in normal controls, higher GABA levels were strongly predictive of longer levels of perceptual suppression and a normal balance of binocular rivalry, but the same relationship did not exist in autistic participants, who experienced disrupted perceptual suppression regardless of GABA levels. Significantly, this indicated a lack of impact from GABA on perceptual suppression in autistic individuals, leading to the supposition that disturbances in the GABAergic signaling pathway (either at the receptor level or due to variations in inhibitor neuronal density) may be the cause of the dysfunction in GABAergic activity.4-6


1.  Robertson CE, Ratia, E-M, Kanwisher N. Reduced GABAergic action in the autistic brain. Current Biology. 2016;26:1-6.

2.  Robertson, CE, Kravits DJ, Freyberg J, et al. Slower rate of binocular rivalry in autism. J Neurosci. 2013;33:16983-16991.

3.  Gaetz W, Bloy, L, Wang, DJ, et al. GABA estimation in the brains of children on the autism spectrum: measurement precision and regional cortical variation. Neuroimage 2014;86, 1–9.

4.  Said CP, and Heeger DJ. A model of binocular rivalry and crossorientation suppression. 2013 Comput. Biol. 9, e1002991.

5.  Fatemi SH, Reutiman TJ, Folsom TD, et al. GABA(A) receptor downregulation in brains of subjects with autism. J Autism Dev Disord. 2009;39, 223–230.

6. Ma DQ, Whitehead PL, Menold MM, et al.  Identification of significant association and gene-gene interaction of GABA receptor subunit genes in autism. Am J Hum Genet. 2005;77,377–388.

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