Wider minicolumns in autism: a neural basis for altered processing?
Previous studies have found alterations in the columnar organization of the cortex in autism spectrum disorders. Such changes have been suggested to be limited to higher order association areas and to spare primary sensory areas. In addition, evidence from gene-expression studies have suggested that there may be an attenuation of cortical differentiation in autism spectrum disorders. The present study specifically assessed the minicolumns of cells that span the depth of the cortex in a larger sample of autism spectrum disorder cases than have been studied previously, and across a broad age range. The cortical regions to be investigated were carefully chosen to enable hypotheses about cortical differentiation and the vulnerability of association cortex to be tested. Measures of the minicolumnar arrangement of the cortex (minicolumn width, spacing and width of the associated axon bundles) were made in four regions of cortex (primary auditory cortex, auditory association cortex, orbital frontal cortex and inferior parietal lobe) for 28 subjects with autism spectrum disorder and 25 typically developing control subjects. The present study found wider minicolumns in autism spectrum disorder [F(1,28) = 8.098, P = 0.008], which was particularly pronounced at younger ages, providing evidence for an altered developmental trajectory at the microstructural level. In addition, altered minicolumn width was not restricted to higher order association areas, but was also seen in the primary sensory region investigated. Finally, this study found evidence that cortical regional differentiation was still present in autism spectrum disorder [F(3,39) = 5.486, P = 0.003], although attenuated compared to typically developing subjects [F(3,45) = 18.615, P < 0.001]. It is suggested that wider spacing of the minicolumns may relate to the enhanced discrimination seen in some individuals with autism spectrum disorders.
1 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK 2 Neuroscience and Mental Health Research Institute, University of Cardiff, CF24 4HQ, UK.
Rebecca
R
McKavanagh
1 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK.
Eleanor
E
Buckley
1 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK steven.chance@ndcn.ox.ac.uk.
Steven A
SA
Chance
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002540:Cerebral Cortex / Q000473:pathology*; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000473:pathology*; D002675:Child, Preschool; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D055815:Young Adult
autism; brain development; enhanced discrimination; minicolumns; primary sensory cortex