Dysfunctional Gamma-band Oscillations in Individuals with Autism Spectrum Disorder

Objective: Autism spectrum disorder (ASD) is a neurodevelopmental disorder involving γ-aminobutyric acid (GABA) neurotransmission. Sensory abnormalities, particularly in the auditory modality, are commonly seen in individuals with ASD. Since GABAergic interneurons play a fundamental role in generating neuronal gamma oscillations, this study aims to investigate whether ASD patients have altered auditory steady-state response (ASSR) in gamma-band range. Methods: We recruited 50 patients with ASD and 41 typically developing controls (TDC). The participants were presented three click trains with rates of stimulation at 20-, 30- and 40-Hz, respectively. The frontal and temporal ASSR was recorded through a 32-channel electrode cap. Evoked power and inter-trial phase coherence (ITC) were derived from the electroencephalogram (EEG) signals. Results: In response to 20-Hz click trains, the ASD group showed lower evoked power at 20-Hz band in the temporal area but higher in the midline frontal area, and lower evoked power at the 30-Hz band in the temporal area. The ASD group showed smaller ITC in the temporal area in response to both 20-Hz anda 30-Hz click trains. There were no significant group differences in the 40-Hz band evoked power and the ITC. When participants were divided into the adult, adolescent and childhood subgroups, all the three groups showed significant differences of frontal 40-Hz band evoked power and between ASD patents and TDC participants. The group differences were observed in bilateral frontal regions in childhood subgroup, but shift to the midline and left frontal regions in the adolescent and adult groups. Conclusion: Age is an important factor to be considered when investigating gamma band auditory steady-state response. Deficits in gamma-band ASSR were noted in patients with ASD, and age was related to the distribution of brain regions where these deficits were found. It provides neuroelectrophysiological evidence for the altered development of GABAergic neurotransmission in patients with ASD.