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Perception is the process by which our brains interpret sensory information. Our brains are constantly evaluating sensory signals in our environments, which shapes how we experience the world and, ultimately, our physical and mental well-being. When this develops differently, it may lead to atypical sensory perception as seen in autism. The addition of sensory symptoms to the most recent diagnostic criteria for autism highlights the need to understand its underlying mechanisms. This thesis used methods from experimental psychology and brain imaging to investigate the neurocognitive mechanisms of perceptual inference in autistic individuals. Chapter 1 introduces the topic of sensory perception, its neurocomputational framework, and its role in autism. It provides an overview of the theories and models of perception in autism and presents the overarching aims of this research. Chapter 2 reports a study of how autistic adults make perceptual decisions on two visual similarity judgment tasks. Signal detection theory analyses indicated that, in both tasks, when compared to typical people, autistic individuals used different decision criteria during conditions of uncertainty. Chapter 3 addresses the limited neuroimaging research on non-social features of autism. Using activation likelihood estimation, findings were condensed from non-social perception task-based functional MRI studies examining differences between autistic and typical participants. Overall, autistic people, compared to typical controls, showed less activity in the prefrontal cortex during perception tasks. More refined analyses revealed that, when compared to typical controls, autistic people showed greater recruitment of the extrastriate cortex during visual processing. Chapters 4 and 5 report findings from a visuomotor probabilistic reversal learning task used to examine how adults with varying levels of autistic traits evaluate sensory information, build, and update sensory expectations. A positive relationship was found between autistic traits and the learning of probable sequences before the reversal. In addition, there were separate main effects of autistic traits and intolerance to uncertainty on the ability to update expectations following the reversal. These findings suggest that, while people with different levels of autistic traits identify statistical regularities at a comparable level to one another, autistic traits play a role in how individuals update their expectations once a change is introduced. Chapter 5 examined how these behavioural findings relate to inhibitory neurotransmitters. In this 7-Tesla MR spectroscopic investigation, γ-Aminobutyric acid (GABA) was measured in the occipital and motor cortices to investigate its role in visuomotor sequential learning and its interactions with autistic traits. Previous findings of a negative relationship between sensorimotor GABA and sequence learning were replicated. At the same time, there were no clear links between autistic traits and occipital and motor GABA. Finally, Chapter 6 ties these findings together and evaluates how they contribute to our understanding of autistic perception. Some of the challenges of cognitive neuroscience research in autism are highlighted alongside clear directions for future work.

Scripts and related files for behavioural tasks

Oxytocin is hypothesized to promote social interactions by enhancing the salience of social stimuli. While previous neuroimaging studies have reported that oxytocin enhances amygdala activation to face stimuli in autistic men, effects in autistic women remain unclear. In this study, the influence of intranasal oxytocin on activation and functional connectivity of the basolateral amygdala – the brain’s “salience detector” – while processing emotional faces vs. shapes was tested in 16 autistic and 21 non-autistic women by fMRI in a placebo-controlled, within-subjects, cross-over design. In the placebo condition, minimal activation differences were observed between autistic and non-autistic women. However, significant drug × group interactions were observed for both basolateral amygdala activation and functional connectivity. Oxytocin increased left basolateral amygdala activation among autistic women (35 voxel cluster, MNI coordinates of peak voxel= -22 -10 -28; mean change=+0.079%, t=3.159, ptukey=0.0166), but not non-autistic women (mean change =+0.003%, t=0.153, ptukey=0.999). Furthermore, oxytocin increased functional connectivity of the right basolateral amygdala with brain regions associated with socio-emotional information processing in autistic women, but not non-autistic women, attenuating group differences in the placebo condition. Taken together, these findings extend evidence of oxytocin’s effects on the amygdala to specifically include autistic women and specify the subregion of the effect.

Background: Oxytocin is hypothesized to promote positive social interactions by enhancing the salience of social stimuli, which may be reflected by altered amygdala activation. While previous neuroimaging studies have reported that oxytocin enhances amygdala activation to emotional face stimuli in autistic men, effects in autistic women remain unclear. Methods: The influence of intranasal oxytocin on neural response to emotional faces vs. shapes were tested in 16 autistic and 21 non-autistic women by fMRI in a placebo-controlled, within-subjects, cross-over design. Effects of group (autistic vs. non-autistic) and drug condition (oxytocin vs. placebo) on the activation and functional connectivity of the basolateral amygdala, the brain’s “salience detector”, were assessed. Relationships between individual differences in autistic-like traits, social anxiety, salivary oxytocin levels, and amygdala activation were also explored.Results: Autistic and non-autistic women showed minimal activation differences in the placebo condition. Significant drug × group interactions were observed for both amygdala activation and functional connectivity. Oxytocin increased left basolateral amygdala activation among autistic women (35 voxel cluster, MNI coordinates of peak voxel = -22 -10 -28; mean change=+0.079%, t=3.159, ptukey=0.0166), but not non-autistic women (mean change =+0.003%, t=0.153, ptukey=0.999). Furthermore, oxytocin increased functional connectivity of the right basolateral amygdala with brain regions associated with socio-emotional information processing in autistic women, but not non-autistic women, thereby attenuating group connectivity differences observed in the placebo condition. Conclusions: This work demonstrates that intranasal oxytocin increases basolateral amygdala activation and connectivity in autistic women while processing emotional faces, which extends and specifies previous findings in autistic men.

To date, neuroimaging research has had a limited focus on non-social features of autism. As a result, neurobi- ological explanations for atypical sensory perception in autism are lacking. To address this, we quantitively condensed findings from the non-social autism fMRI literature in line with the current best practices for neu- roimaging meta-analyses. Using activation likelihood estimation (ALE), we conducted a series of robust meta- analyses across 83 experiments from 52 fMRI studies investigating differences between autistic (n = 891) and typical (n = 967) participants. We found that typical controls, compared to autistic people, show greater activity in the prefrontal cortex (BA9, BA10) during perception tasks. More refined analyses revealed that, when compared to typical controls, autistic people show greater recruitment of the extrastriate V2 cortex (BA18) during visual processing. Taken together, these findings contribute to our understanding of current theories of autistic perception, and highlight some of the challenges of cognitive neuroscience research in autism