Adaptation is a fundamental property of cortical neurons and has been suggested to be altered in individuals with autism spectrum disorder (ASD). We used fMRI to measure adaptation induced by repeated audio-visual stimulation in early sensory cortical areas in individuals with ASD and neurotypical (NT) controls. The initial transient responses were equivalent between groups in both visual and auditory cortices and when stimulation occurred with fixed-interval and randomized-interval timing. However, in auditory but not visual cortex, the post-transient sustained response was greater in individuals with ASD than NT controls in the fixed-interval timing condition, reflecting reduced adaptation. Further, individual differences in the sustained response in auditory cortex correlated with ASD symptom severity. These findings are consistent with hypotheses that ASD is associated with increased neural responsiveness but that responsiveness differences only manifest after repeated stimulation, are specific to the temporal pattern of stimulation, and are confined to specific cortical regions.

Response inhibition is a main function of cognitive control and its neural substrates have been studied extensively. However, it is still a question whether previous brain imaging investigations were successful in isolating specific response inhibition activation. In the current study we attempted to pinpoint response inhibition in the brain using a Go/No-go task and fMRI, by contrasting rare-No-go trials with prevalent-No-go trials. Although inhibition is required in all No-go trials, task variants with rare-No-go cases (25%) create a prepotent response which elicits a strong demand for inhibition, while task variants with prevalent-No-go cases (75%) require very little inhibition effort. Since the neural activation in this design is extracted solely from No-go trials, differing only in the extent of inhibitory demand, the analysis avoids contamination of the data with motor effects or visual factors. Using this experimental design we highlight the contribution of the parietal cortex (bilaterally) to inhibitory processes, while casting doubts about the specificity of frontal activation in such processes. Future studies are required to verify that bilateral intraparietal sulcus and left temporo-parietal junction activations could be markers of inhibitory control.

The importance of sex as a biological variable has recently been emphasized by major funding organizations [1] and within the neuroscience community [2]. Critical sex-based neural differences are indicated by, for example, conditions such as autism spectrum disorder (ASD) that have a strong sex bias with a higher prevalence among males [51, 3]. Motivated by this broader context, we report a marked sex difference in a visual motion perception task among neurotypical adults. Motion duration thresholds [4, 5]-the minimum duration needed to accurately perceive motion direction-were considerably shorter for males than females. We replicated this result across three laboratories and 263 total participants. This type of enhanced performance has previously been observed only in special populations including ASD, depression, and senescence [6-8]. The observed sex difference cannot be explained by general differences in speed of visual processing, overall visual discrimination abilities, or potential motor-related differences. We also show that while individual differences in motion duration thresholds are associated with differences in fMRI responsiveness of human MT+, surprisingly, MT+ response magnitudes did not differ between males and females. Thus, we reason that sex differences in motion perception are not captured by an MT+ fMRI measure that predicts within-sex individual differences in perception. Overall, these results show how sex differences can manifest unexpectedly, highlighting the importance of sex as a factor in the design and analysis of perceptual and cognitive studies.

The balance of excitation and inhibition in neural circuits is hypothesized to be increased in autism spectrum disorder, possibly mediated by altered signaling of the inhibitory neurotransmitter γaminobutyric acid (GABA), yet empirical evidence in humans is inconsistent. We used edited magnetic resonance spectroscopy (MRS) to quantify signals associated with both GABA and the excitatory neurotransmitter glutamate in multiple regions of the sensory and sensorimotor cortex, including primary visual, auditory, and motor areas in adult individuals with autism and in neurotypical controls. Despite the strong a priori hypothesis of reduced GABA in autism spectrum disorder, we found no group differences in neurometabolite concentrations in any of the examined