![]() The article also notes the ubiquitous role of gating by basal ganglia loops in regulating all the functions that iSTART models. These repetitive behaviors may be ameliorated by drugs that augment D2 dopamine receptor responses or reduce D1 dopamine receptor responses. 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 behaviors may be ameliorated by operant conditioning methods. 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. 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. 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. 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. 2Department of Biomedical Engineering, Boston University, Boston, MA, United States. ![]() 1Center for Adaptive Systems, Graduate Program in Cognitive and Neural Systems, Departments of Mathematics & Statistics, Psychological & Brain Sciences, and Biomedical Engineering, Boston University, Boston, MA, United States.
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