Alterations in the organization of the isocortical layer I in trisomy 22.
The isocortical layer I of human fetal brains obtained from different cases of chromosomal abnormalities (trisomy 18, 21, 22) and controls without pathological disturbances were investigated histologically and immunohistochemically by using the antibodies SMI 311, SMI 35 and SMI 81 (SNAP 25) as well as antibodies against GAP 43 and calretinin. In cases of trisomy 22 the Cajal-Retzius cells in Nissl-sections and in SMI 311-immunopreparations do not reveal any alterations regarding their location or morphology. However, the axonal plexus, selectively labelled with SMI 35, normally located in layer Ib, is malpositioned in Ia. Likewise, SNAP 25- and GAP 43-immunoreactive structures, which were taken as signs of synaptogenesis, are displaced and appear in Ia instead of Ib. Cases of trisomy 18 and 21 show no changes within the organization of layer I. In trisomy 22 the isocortical layer I reveals malpositioned axonal plexus and a corresponding displacement of synaptic proteins. The possible significance of this alteration in the developmental process of the isocortex is discussed.
Ulfig
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Department of Anatomy, University of Rostock, Germany. norbert.ulfig@med.uni-rostock.de
Tietz
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B
Bohl
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J
D001921:Brain / Q000196:embryology* / Q000473:pathology; D064032:Calbindin 2; D002869:Chromosome Aberrations / Q000196:embryology / Q000235:genetics / Q000473:pathology*; D025063:Chromosome Disorders; D002887:Chromosomes, Human, Pair 18; D002891:Chromosomes, Human, Pair 21; D002892:Chromosomes, Human, Pair 22; D004314:Down Syndrome / Q000235:genetics; D005333:Fetus; D019922:GAP-43 Protein / Q000032:analysis; D006801:Humans; D009419:Nerve Tissue Proteins / Q000032:analysis*; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D014314:Trisomy
C576764:CALB2 protein, human; D064032:Calbindin 2; D019922:GAP-43 Protein; D009419:Nerve Tissue Proteins; D064030:S100 Calcium Binding Protein G