doi:10.1016/j.expneurol.2004.11.024 
Copyright © 2004 Elsevier Inc. All rights reserved.
Development of interlaminar astroglial processes in the cerebral cortex of control and Down's syndrome human cases
Jorge A. Colomboa, 
, 
, Hernán D. Reisina, Marta Jonesb and Carolina Benthama
aUnidad de Neurobiología Aplicada (CEMIC-CONICET), Av. Galván 4102, 1431 Cdad. Buenos Aires, Argentina
bHospital Interzonal Especializado en Pediatría (HIEP), La Plata, Provincia de Buenos Aires, Argentina
Received 15 July 2004;
revised 8 October 2004;
accepted 29 November 2004.
Available online 16 February 2005.
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Abstract
Glial cytoarchitecture in human cerebral cortex is constituted by two overlapping layouts: the (general mammalian) “glial syncytium” and the (primate-specific) “interlaminar glial palisade” (IGP) composed by astroglial cells, with long, radial processes that traverse several supragranular layers. In this study, the emergence and early organization of the IGP was analyzed using immunocytochemical procedures in postmortem infantile human control and age matched, Down's syndrome (DS) cases. In control cases, first signs of a radial array of unbranched astroglial processes were apparent at the end of the period of “physiological astrocytosis” (20–40 days of postnatal life), and its general profile (except perhaps the density of cell processes) reached the adultlike configuration by the second month of life. The initial organization of the IGP was similar in control and DS cases, although a breakdown in DS became manifest by the first year of age, or earlier, albeit with individual variations. These changes tended to evolve in a “mosaic” fashion and included partial disruption of the palisade, or persistence of the “physiological astrocytosis”. These observations were compared against samples from elder DS cases with an Alzheimer's type of dementia (AtD). Collectively, results suggest that DS also involves astroglial alterations during early stages of brain development, and that those changes progress with age, until an AtD ensues during adult life.
Keywords: Corticogenesis; Primate's brain; Glia; GFAP
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Fig. 1. Development of GFAP-immunoreactive astroglia in the cerebral cortex of early postnatal control human cases; also Vim-immunoreactive astroglia in (C). (A) Sixteen days old, parietal postcentral cortex. Note aligned remnants of radial glia (“transforming glia”). (B) Twenty days old, frontal motor cortex. (C) Twenty days old, parietal postcentral cortex. (D) Twenty days old, frontal cortex, region of Broca. (E) Twenty-eight days old, calcarine cortex, layer I. (F) Forty days old, frontal cortex, region of Broca. (G) Forty days old, parietal postcentral cortex. (H) Forty days old, cortex of the middle temporal gyrus. Note astrocytosis in a 20-day-old case, and the emergence of interlaminar processes in the 40-day-old case. Broken line indicates the depth of layer I. (I) Two months old, frontal precentral (motor) cortex. (J) Six months old, calcarine cortex. (K) Six months old, orbital prefrontal cortex. (L) Two years old, inferior (angular) parietal cortex. Scale bars: in (A and I) 100 μm, also for (B–D, F,G, J–L); 100 μm in (E); 300 μm in (H).
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Fig. 2. Presence of the IGP in the cerebral cortex of control (left panel) and DS (right panel) infant and adult human cases. The pattern of the IGP is graphically represented as percentages of three categories classified as: “complete” palisade (solid bars), “incomplete” (gray bars), and “absent” (empty bars). Due to limited sample availability, a comparative analysis of matching cortical regions was only possible for the following regions: prefrontal dorsolateral, frontal precentral (motor), and calcarine. (A) Calcarine cortex; (B) dorsolateral prefrontal cortex; (C) precentral frontal cortex. d = days, m = months, y = years of age. In order to make all panels visually comparable, an identical age axis was construed. Circles indicate lack of data. Arrows indicate cases with Alzheimer-type dementia. (D). Overall average percentage of IGP completeness, for infants and adults. Note that control cases have similar patterns for both age groups. In DS group, the proportion of complete IGP is severely reduced with age. Asterisk indicates significant differences (P < 0.001; χ2 test) between connected pairs.
Fig. 3. Graphic representation of “palisade's” depth (mean ± SE; in μm) of three cortical areas of the cerebral cortex in control and DS infant cases (younger than 46 months). Mean values of control and DS cases for each region are indicated by solid and broken lines, respectively (average values from cases older than 2 months, inclusive). Number of measurements are indicated between brackets. Asterisk indicates statistical differences (P < 0.001; t test) between control and DS cases in (B). No statistical differences were found between control and DS cases in (A) or in (C). (A) Calcarine cortex. (B) Dorsolateral prefrontal cortex. (C) Precentral frontal cortex. d = days, m = months, y = years of age.
Fig. 4. Spatial organization of interlaminar processes from control (filled symbols) and DS (empty symbols). (A) Tortuosity (mean) of individual interlaminar processes from calcarine (circles), dorsolateral prefrontal (triangles), and precentral frontal (squares) cerebral cortex. In general, there is a marked overlap of average values for all cortical areas. There was a lack of any clear age-dependent distribution for individual processes tortuosity. (B) Parallelism (mean) of the IGP. Note the general tendency of average values towards a more parallel arrangement with age for infantile cases, and a decay (less parallel palisades) for elder cases.
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Fig. 5. Alterations of GFAP-IR glial processes in the cerebral cortex of DS cases. (A) Three months old, frontal precentral (motor) cortex. (B) Three months old (same case as in A), calcarine cortex. (C) Three months old (same case as in A), prefrontal cortex. (D) Five months old, calcarine cortex. (E) Five months old, precentral frontal cortex. (F) Twenty-four months old, prefrontal cortex. (G) Twenty-seven months old, precentral (motor) cortex. (H) Twenty-four years old, prefrontal cortex. (I) Same case as in (H), calcarine cortex. (J) Same case and area, as in (I), another locus. Note variations in density and depth of the interlaminar “palisade” with respect to panel I. (K) Sixty-nine years old, DS with Alzheimer type of dementia, postcentral parietal cortex. (L) Same case as in (K), precentral frontal cortex, layer I. Note complete disappearence of the IGP in (K) and (L). Broken line indicates the depth of layer I. Variations in the overall background gray tones of the figures (mostly in A–J) were due to changes in optical tissue densities secondary to exposure to rescue procedures. Scale bars: 100 μm in (A and G) also for (B–K); 100 μm in (L).
Table 1.
List of control cases included in the present study
Postnatal age: d = days; m = months; y = years. Gender: M for male, F for female. Postmortem time (PM) before fixation in hours. +, ++ = degree of autolysis (A) or granular degeneration. nd = non detectable. NA = not available.
Table 2.
List of DS cases included in the present study
Postnatal age: d = days; m = months; y = years. Gender: M for male, F for female. Postmortem time (PM) before fixation in hours. +, ++ = degree of autolysis (A) or granular degeneration. nd = non detectable. NA = not available.
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