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The brain of the bottlenose dolphin exhibits patterns of isocortical parcellation and cytoarchitecture distinct from those seen in primates, yet cell clusters in anterior insula are comparable in scale to module-like cell arrangements found throughout isocortex in other placental mammalian species with long divergent evolutionary histories. This similarity may be due to common ancestry, or to convergence as a result of selective constraints on organization of connections within such modules. Differences reflect alternate arrangements of minicolumns, an elemental cytoarchitectonic motif of isocortex defined by radially oriented pyramidal cell arrays. In contrast with larger modular structures incorporating them, minicolumns have been highly conserved in mammalian evolution. In this study a previously validated imaging method was employed to assess verticality, D, a parameter indicating radial bias of isocortex. Photomicrographs of coronal Nissl-stained sections of dolphin anterior insular cortex were compared with sections from human brains of putatively homologous areas as well as other isocortical areas differing in modular organization. Dolphin insula exhibited a high degree of verticality consistent with conserved minicolumnar organization. Our findings indicate that a basic structural motif of isocortex is synapomorphic in a species of marine mammal exhibiting unique phylogenetically derived isocortical characteristics.

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The minicolumn derives from the radial migration of neurons along glial scaffoldings during gestation. Investigators have presumed the minicolumn to be a single-cell wide structure based on their rectilinear migratory origin. The present study measures the width of minicolumnar cores in both supra- and infra-granular layers. Postmortem tissue was obtained from 9 brain areas in 7 normative individuals. Examined tissues were celloidin embedded and Nissl stained. Digital images were denoised and then analyzed with a step-wise algorithm involving region growing and recursive line tracing. Significant differences were noted between the minicolumnar core widths of supra- and infra-granular layers. A review of the literature on corticogenesis provides some ideas as to how these laminar differences in minicolumnar core width are engendered.

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To explain the pattern of preserved and superior abilities found in autism spectrum disorders, a hypothesis has emerged, which assumes that there is a developmental bias towards the formation of short-range connections. This would result in excessive activity and overconnectivity within susceptible local networks. These networks might become partially isolated and acquire novel functional properties. In turn, this would affect the formation of long-range circuits and systems governing top-down control and integration. Despite many tantalizing clues, mechanisms relating pathogenesis and altered cell function to the 'disconnection' of integrative and focal activity remain obscure. However, recent post-mortem studies of brains of individuals with autism have shown characteristic differences in the morphometry of radial cell minicolumns, which add credence to the connectivity hypothesis.

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Radially oriented ensembles of neurons and their projections, termed minicolumns, are hypothesized to be the basic microcircuit of mammalian cerebral cortex. Minicolumns can be divided into a core and a peripheral neuropil space compartment. The core of minicolumns is constrained by the migratory path of pyramidal cells and their attendant radially oriented projections. Variation in minicolumnar morphometry and density is observed both within and across species. Using a scale-independent measure of variability in minicolumnar width (V(CW)), we demonstrated a significant increase in V(CW) in layers III-V of striate cortex in humans relative to macaques and chimpanzees. Despite changes in minicolumnar width (CW) across species, their core space (w) remained the same. Given that cellular elements and processes within the peripheral neuropil space of minicolumns are derived from assorted sources, cross-species differences in VCW may result from genetic and epigenetic influences acting primarily on this compartment of the minicolumn.

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It has been postulated that the prefrontal cortices of schizophrenic patients have significant alterations in their neuropil space. However, previous results have been contradictory and inconclusive, reporting both decreases and increases in the prefrontal neuropil. The present study re-examines these findings based on measurements of cell density, and inter-cellular distances within and between cell minicolumns. The results indicate alterations in the neuropil of schizophrenic patients according to both the lamina and cortical area examined. Alterations were present in all cortical areas studied. The findings suggest an alteration in the modulatory systems innervating the cell minicolumn. Furthermore, the lack of variation in core columnarity parameters argues in favor of a defect post-dating the formation of the cell minicolumn.

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It has been suggested that the cell minicolumn is the smallest module capable of information processing within the brain. In this case series, photomicrographs of six regions of interests (Brodmann areas 4, 9, 17, 21, 22, and 40) were analyzed by computerized image analysis for minicolumnar morphometry in the brains of three distinguished scientists and six normative controls. Overall, there were significant differences (p < 0.001) between the comparison groups in both minicolumnar width (CW) and mean cell spacing (MCS). Although our scientists did not exhibit deficits in communication or interpersonal skills, the resultant minicolumnar phenotype bears similarity to that described for both autism and Asperger's syndrome. Computer modeling has shown that smaller columns account for discrimination among signals during information processing. A minicolumnar phenotype that provides for discrimination and/or focused attention may help explain the savant abilities observed in some autistic people and the intellectually gifted.

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Radial translaminar arrays of pyramidal cells-minicolumns-are a pervasive structural motif of placental mammalian neocortex, which are anticipated in the earliest stages of cortical development by the formation of ontogenetic cell columns comprising radial glial cells and associated radially migrating neurons. In the present study we examine the temporal continuity in these structures throughout development and aging. Computerized image analysis of micrograph Nissl-stained postmortem tissue produced estimates of the median free path through neuropil in the radial direction (parallel to pyramidal cell arrays) and in the tangential direction (parallel to the cortical surface). These data were modeled as a biphasic power law with respect to in utero development and postnatal age, multiplied by a decay factor. No significant change in the ratio of radial to tangential neuropil space was demonstrated in either the prenatal or postnatal sample population. Neuropil development follows a prenatal phase of cubic volumetric growth with a postnatal phase of linear volumetric growth. The data suggest the continuity of columnar structures from early in gestation through postnatal maturation.

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In this study, we employed morphometric image analysis of the hippocampus proper and temporal lobe neocortex in postmortem tissue to determine vertical bias quantified as Deltatheta, angular dispersion, as well asan index of alignment of cellular elements relative to the radial plane. The radial alignment of cellular elements was consistent with a minicolumnar organization of the cortex. Photomicrographs were taken of the left-hemisphere hippocampal CA3/1 subfields of 13 fetal subjects ranging in gestational age from 19 weeks to 36 weeks and 19 normal individuals aged 4 months to 98 years. For comparison, micrographs from the temporal lobe (Brodmann areas 21 and 22) were similarly processed for layers III and V, where the x-axes of the transformed coordinate system were taken to be the layer III/IV and IV/V borders, respectively. Computerized image analysis measurements of the angular dispersion for the temporal lobe region and hippocampus proper differed significantly within the same brains (p < 0.001). The neocortical layer III exhibited the highest values for Deltatheta, indicating a high degree of columnar organization. Values for Deltatheta in the hippocampal CA subfields were lower but demonstrated significance for the radial alignment of neurons in this area. Values for Deltathetain layer V were intermediate between those of layer III and the hippocampus, consistent with increasing degrees of radial columnar organization of infragranular layers of the neocortex in comparison with the hippocampus and of supragranular in comparison with infragranular neocortical layers. Pyramidal cell arrays within allocortical areas and the neocortex constitute different modular arrangements. This morphological variability may be the expression of evolutionary differences in cortical development.

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Autism is characterized by qualitative abnormalities in behavior and higher order cognitive functions. Minicolumnar irregularities observed in autism provide a neurologically sound localization to observed clinical and anatomical abnormalities. This study corroborates the initial reports of a minicolumnopathy in autism within an independent sample. The patient population consisted of six age-matched pairs of patients (DSM-IV-TR and ADI-R diagnosed) and controls. Digital micrographs were taken from cortical areas S1, 4, 9, and 17. The image analysis produced estimates of minicolumnar width (CW), mean interneuronal distance, variability in CW (V (CW)), cross section of Nissl-stained somata, boundary length of stained somata per unit area, and the planar convexity. On average CW was 27.2 microm in controls and 25.7 microm in autistic patients (P = 0.0234). Mean neuron and nucleolar cross sections were found to be smaller in autistic cases compared to controls, while neuron density in autism exceeded the comparison group by 23%. Analysis of inter- and intracluster distances of a Delaunay triangulation suggests that the increased cell density is the result of a greater number of minicolumns, otherwise the number of cells per minicolumns appears normal. A reduction in both somatic and nucleolar cross sections could reflect a bias towards shorter connecting fibers, which favors local computation at the expense of inter-areal and callosal connectivity.

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The developing forebrain exhibits a high degree of spatiotemporal regulation of proliferation and cell cycle exit in progenitor cells of its proliferative zones. This results in the balanced deployment of progenitors between asymmetric division, yielding postmitotic neurons and cycling progenitors, and terminal symmetric division, resulting in differentiated daughter cells. Radial glia have been demonstrated to be the principal neuronal progenitor of the cortical primordium. Lineage tracing studies employing real-time imaging in vivo have enhanced understanding of neuronal production and migration. Cortical projection neurons have been shown to arise from the radial migration of precursors generated in the dorsal telencephalon, whereas most interneurons derive from the germinal zone of the ventral telencephalon and migrate tangentially into the primordial cortex. Cells from both populations undergo diverse and complex sequences of migratory activity. Neuronal phenotypic potential is informed in progenitors prior to their last cell division. Laminar and regional fate potential of progenitors becomes progressively restricted with successive cell cycles. This process of neuronal fate specification is regulated by the interaction of programs of transcriptional regulation with extrinsic patterning signals according to time and region of the proliferative zone in which the final mitotic cycle occurs.

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