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The Neuroscientist, Vol. 9, No. 6, 496-507 (2003)
DOI: 10.1177/1073858403253552

Disruption in the Inhibitory Architecture of the Cell Minicolumn: Implications for Autisim

Manuel F. Casanova

Department of Psychiatry and Department of Neurology, Pathology, Anatomy and Cell Biology; Medical College of Georgiam0casa02{at}louisville.edu

Daniel Buxhoeveden

Department of Psychiatry, Medical College of Georgia

Juan Gomez

Department of Psychiatry, Medical College of Georgia

The modular arrangement of the neocortex is based on the cell minicolumn: a self-contained ecosystem of neurons and their afferent, efferent, and interneuronal connections. The authors’ preliminary studies indicate that minicolumns in the brains of autistic patients are narrower, with an altered internal organization. More specifically, their minicolumns reveal less peripheral neuropil space and increased spacing among their constituent cells. The peripheral neuropil space of the minicolumn is the conduit, among other things, for inhibitory local circuit projections. A defect in these GABAergic fibers may correlate with the increased prevalence of seizures among autistic patients. This article expands on our initial findings by arguing for the specificity of GABAergic inhibition in the neocortex as being focused around its mini- and macrocolumnar organization. The authors conclude that GABAergic interneurons are vital to proper minicolumnar differentiation and signal processing (e.g., filtering capacity of the neocortex), thus providing a putative correlate to autistic symptomatology.

Key Words: Autistic disorder • Cerebral cortex/pathology • Computer simulation


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