Abstract
Intro: The primary agent of inhibitory neurotransmission in visual cortex, GABA, has been linked to autism etiology in animal, genetic, and post-mortem studies. Specifically, GABA is thought to be down-regulated in the autistic brain, producing an overabundance of excitatory neurotransmission. Yet, perturbations in GABAergic signaling have never been experimentally associated with behavioral symptoms in people with autism. We recently demonstrated a striking autistic deficit in binocular rivalry (Robertson et al., 2013), a visual behavior that is governed by Excitatory/Inhibitory dynamics in the brain. Here, we tested whether the dynamics of binocular rivalry in typical adults are correlated with levels of excitatory (glutamate) and inhibitory (GABA) neurotransmitters measured in vivo. Methods: We measured binocular rivalry dynamics in 18 control participants, as well as the concentration of excitatory (glutamate) and inhibitory (GABA) neurotransmitters in the primary visual (test) and motor (control) areas of each individual’s brain using Magnetic Resonance Spectroscopy (MRS). Results: GABA in V1 strongly predicted the dynamics of binocular rivalry in control individuals (Proportion of mixed percepts: rho = -0.61, p < 0.008) – where less GABA predicted slower binocular rivalry dynamics with longer mixed percepts, corresponding to the atypical dynamics we previously observed in ASD. This relationship was observed for rivalry using both simple (gratings) and complex stimuli (objects) (both r < -0.6, p < 0.009). Further, these results were specific to visual cortex: while GABA concentration in M1 predicted performance on a Go/No-Go motor task (rho = 0.67, p < 0.002), it did not predict rivalry dynamics (rho = -0.35,p > 0.19). Conclusions: Here, we demonstrate that a robust behavioral alteration in individuals with ASD strongly predicts GABA concentration measured in controls. This research may lead to the first experimental demonstration of a link between a robust autistic symptom and a prominent theory of autistic neural circuitry.
Meeting abstract presented at VSS 2015