An examination of the cortical subplate and synaptic spine morphology in autism: microanatomical evidence for underconnectivity
AuthorAvino, Thomas A.
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The subplate is a subcortical compartment situated at the interface between cortical gray and white matter in the human brain (and other mammalian species). The subplate and its constituent neurons play a very important role during neurodevelopment in constructing proper cortical circuitry, especially in guiding connections to and from the thalamus. Many subplate neurons die following these developmental processes, while some become embedded into the mature circuitry and act as "amplifiers" or "modulators" of cortical signals. An excessive presence of these neurons has been shown in other neurological disorders such as schizophrenia and seizure disorder and is hypothesized to cause functional disconnectivity in the mature brain. Recently, autism has been conceived as a disorder of abnormal cortical connectivity, which has been shown in a number of functional imaging studies however, the microanatomical substrate(s) for which this underconnectivity is occurring is poorly understood. The goal of the present study was to assess potential microanatomical underpinnings of underconnectivity in autism through a systematic investigation of the neurons of the cortical subplate in addition to an examination of synaptic spine morphology in the cerebral cortex. The results show that individuals with autism show an increased density of subplate neurons in the parietal lobe and furthermore, the morphology of these neurons in the cortical subplate in autism deviates from their neurotypical counterparts. The results also show abnormal synaptic spine morphology on cortical pyramidal cells in individuals with autism demonstrating a lack of connectional strength at these synapses. The findings presented here provide two mechanisms at the cellular and synaptic level for which disrupted cortical connectivity may be occurring in autism. Moreover, the findings provide evidence for a specific neurodevelopmental alteration in autism that is prenatal in origin. The results have implications for future research, diagnoses, and treatments for the disorder.