Abstract
This article develops the iSTART neural model that proposes how specific imbalances in cognitive, emotional, timing, and motor processes that involve brain regions like prefrontal cortex, temporal cortex, amygdala, hypothalamus, hippocampus, and cerebellum may interact together to cause behavioral symptoms of autism. These imbalances include underaroused emotional depression in the amygdala/hypothalamus, learning of hyperspecific recognition categories that help to cause narrowly focused attention in temporal and prefrontal cortices, and breakdowns of adaptively timed motivated attention and motor circuits in the hippocampus and cerebellum. The article expands the model’s explanatory range by, first, explaining recent data about Fragile X syndrome (FXS), mGluR, and trace conditioning; and, second, by explaining distinct causes of stereotyped behaviors in individuals with autism. Some of these stereotyped behaviors, such as an insistence on sameness and circumscribed interests, may result from imbalances in the cognitive and emotional circuits that iSTART models. These behaviors may be ameliorated by operant conditioning methods. Other stereotyped behaviors, such as repetitive motor behaviors, may result from imbalances in how the direct and indirect pathways of the basal ganglia open or close movement gates, respectively. These repetitive behaviors may be ameliorated by drugs that augment D2 dopamine receptor responses or reduce D1 dopamine receptor responses. The article also notes the ubiquitous role of gating by basal ganglia loops in regulating all the functions that iSTART models.
Highlights
The core symptoms of autism spectrum disorder have been defined clinically to include deficits in social communication with regards to social reciprocity, communication toward social interaction, and skills required to develop, maintain and understand relationships
This paper provides a self-contained heuristic overview of relevant computational principles, mechanisms, circuits, and architectures that follow from the above strategy
The article proposes how quantitative neural models of normal behaviors can generate symptoms of Fragile X syndrome (FXS) and autistic repetitive behaviors when their mechanisms become imbalanced in prescribed ways
Summary
The core symptoms of autism spectrum disorder have been defined clinically to include deficits in social communication with regards to social reciprocity, communication toward social interaction, and skills required to develop, maintain and understand relationships. These mechanisms include category learning, reinforcement learning, and adaptively timed learning. Repetitive behaviors may be caused in individuals who are kept in restricted environments, due to how these environments curtail normal operant behaviors It is explained how RMBs, such as movement gaits and saccade staircases, may be caused in normal individuals when basal ganglia gates in the SNr (Figure 2), remain open so long that downstream recurrent circuits can persistently oscillate and thereby cause RMBs. Imbalances between the direct and indirect pathways in the basal ganglia of individuals with autism (Figure 2) may cause sustained opening of basal ganglia gates, thereby triggering. These repetitive behaviors may be ameliorated by treatments that augment D2 dopamine receptor responses or reduce D1 dopamine receptor responses
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