Faculty Opinions recommendation of Absence of Cajal-Retzius cells and subplate neurons associated with defects of tangential cell migration from ganglionic eminence in Emx1/2 double mutant cerebral cortex.

2002 ◽  
Author(s):  
Christopher A Walsh
Keyword(s):  
Cerebral Cortex ◽  
Cell Migration ◽  
Double Mutant ◽  
Ganglionic Eminence ◽  
Subplate Neurons ◽  
Retzius Cells

Absence of Cajal-Retzius cells and subplate neurons associated with defects of tangential cell migration from ganglionic eminence in Emx1/2 double mutant cerebral cortex

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3479-3492 ◽  
Author(s):  
Koji Shinozaki ◽  
Toshihiko Miyagi ◽  
Michio Yoshida ◽  
Takaki Miyata ◽  
Masaharu Ogawa ◽  
...  
Keyword(s):  
Double Mutant ◽  
Cell Number ◽  
Cortical Plate ◽  
Ganglionic Eminence ◽  
Tetraploid Cell ◽  
Radial Glial Cells ◽  
Gap Gene ◽  
Germinal Zone ◽  
Subplate Neurons ◽  
Retzius Cells

Emx1 and Emx2, mouse orthologs of the Drosophila head gap gene, ems, are expressed during corticogenesis. Emx2 null mutants exhibit mild defects in cortical lamination. Segregation of differentiating neurons from proliferative cells is normal for the most part, however, reelin-positive Cajal-Retzius cells are lost by the late embryonic period. Additionally, late-born cortical plate neurons display abnormal position. These types of lamination defects are subtle in the Emx1 mutant cortex. In the present study we show that Emx1 and Emx2 double mutant neocortex is much more severely affected. Thickness of the cerebral wall was diminished with the decrease in cell number. Bromodeoxyuridine uptake in the germinal zone was nearly normal; moreover, no apparent increase in cell death or tetraploid cell number was observed. However, tangential migration of cells from the ganglionic eminence into the neocortex was greatly inhibited. The wild-type ganglionic eminence cells transplanted into Emx1/2-double mutant telencephalon did not move to the cortex. MAP2-positive neuronal bodies and RC2-positive radial glial cells emerged normally, but the laminar structure subsequently formed was completely abnormal. Furthermore, both corticofugal and corticopetal fibers were predominantly absent in the cortex. Most importantly, neither Cajal-Retzius cells nor subplate neurons were found throughout E11.5-E18.5. Thus, this investigation suggests that laminar organization in the cortex or the production of Cajal-Retzius cells and subplate neurons is interrelated to the tangential movement of cells from the ganglionic eminence under the control of Emx1 and Emx2.

The role of Pax6 in restricting cell migration between developing cortex and basal ganglia

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5569-5579 ◽  
Author(s):  
P. Chapouton ◽  
A. Gartner ◽  
M. Gotz
Keyword(s):  
Cerebral Cortex ◽  
Cell Migration ◽  
Basal Ganglia ◽  
Fluorescent Protein ◽  
Ganglionic Eminence ◽  
Cortical Cells ◽  
Dorsal Telencephalon ◽  
Essential Function ◽  
Green Fluorescent

It is not clear to what extent restricted cell migration contributes to patterning of the developing telencephalon, since both restricted and widespread cell migration have been observed. Here, we have analysed dorso-ventral cell migration in the telencephalon of Pax6 mutant mice (Small Eye). The transcription factor Pax6 is expressed in the dorsal telencephalon, the cerebral cortex. Focal injections of adenoviral vectors containing the green fluorescent protein were used to follow and quantify cell movements between two adjacent regions in the developing telencephalon, the cerebral cortex and the ganglionic eminence (the prospective basal ganglia). The analysis in wild-type mice confirmed that the cortico-striatal boundary acts as a semipermeable filter and allows a proportion of cells from the ganglionic eminence to invade the cortex, but not vice versa. Ventro-dorsal cell migration was strongly enhanced in the Pax6 mutant. An essential function of Pax6 in the regionalisation of the telencephalon is then to limit the invasion of the cortex by cells originating in the ganglionic eminence. Cortical cells, however, remain confined to the cortex in the Pax6 mutant. Thus, dorsal and ventral cells are restricted to their respective territories by distinct mechanisms.

Disabled-1 acts downstream of Reelin in a signaling pathway that controls laminar organization in the mammalian brain

Development ◽  
1998 ◽  
Vol 125 (18) ◽  
pp. 3719-3729 ◽  
Author(s):  
D.S. Rice ◽  
M. Sheldon ◽  
G. D'Arcangelo ◽  
K. Nakajima ◽  
D. Goldowitz ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Signaling Pathway ◽  
Developmental Process ◽  
Cortical Plate ◽  
Mammalian Brain ◽  
Granule Neurons ◽  
Adapter Protein ◽  
Cell Position ◽  
Neuronal Precursors ◽  
Retzius Cells

Mutation of either reelin (Reln) or disabled-1 (Dab1) results in widespread abnormalities in laminar structures throughout the brain and ataxia in reeler and scrambler mice. Both exhibit the same neuroanatomical defects, including cerebellar hypoplasia with Purkinje cell ectopia and disruption of neuronal layers in the cerebral cortex and hippocampus. Despite these phenotypic similarities, Reln and Dab1 have distinct molecular properties. Reln is a large extracellular protein secreted by Cajal-Retzius cells in the forebrain and by granule neurons in the cerebellum. In contrast, Dab1 is a cytoplasmic protein which has properties of an adapter protein that functions in phosphorylation-dependent intracellular signal transduction. Here, we show that Dab1 participates in the same developmental process as Reln. In scrambler mice, neuronal precursors are unable to invade the preplate of the cerebral cortex and consequently, they do not align within the cortical plate. During development, cells expressing Dab1 are located next to those secreting Reln at critical stages of formation of the cerebral cortex, cerebellum and hippocampus, before the first abnormalities in cell position become apparent in either reeler or scrambler. In reeler, the major populations of displaced neurons contain elevated levels of Dab1 protein, although they express normal levels of Dab1 mRNA. This suggests that Dab1 accumulates in the absence of a Reln-evoked signal. Taken together, these results indicate that Dab1 functions downstream of Reln in a signaling pathway that controls cell positioning in the developing brain.

scholarly journals The Medial Ganglionic Eminence Gives Rise to a Population of Early Neurons in the Developing Cerebral Cortex

1999 ◽  
Vol 19 (18) ◽  
pp. 7881-7888 ◽  
Author(s):  
Alexandros A. Lavdas ◽  
Maria Grigoriou ◽  
Vassilis Pachnis ◽  
John G. Parnavelas
Keyword(s):  
Cerebral Cortex ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence

scholarly journals Thyroid hormone regulated genes in cerebral cortex development

2017 ◽  
Vol 232 (2) ◽  
pp. R83-R97 ◽  
Author(s):  
Juan Bernal
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormones ◽  
Fetal Development ◽  
Cell Types ◽  
Control Of Gene Expression ◽  
Cellular Targets ◽  
Cerebral Cortex Development ◽  
Subplate Neurons ◽  
Genes Encoding

The physiological and developmental effects of thyroid hormones are mainly due to the control of gene expression after interaction of T3 with the nuclear receptors. To understand the role of thyroid hormones on cerebral cortex development, knowledge of the genes regulated by T3 during specific stages of development is required. In our laboratory, we previously identified genes regulated by T3 in primary cerebrocortical cells in culture. By comparing these data with transcriptomics of purified cell types from the developing cortex, the cellular targets of T3 can be identified. In addition, many of the genes regulated transcriptionally by T3 have defined roles in cortex development, from which the role of T3 can be derived. This review analyzes the specific roles of T3-regulated genes in the different stages of cortex development within the physiological frame of the developmental changes of thyroid hormones and receptor concentrations in the human cerebral cortex during fetal development. These data indicate an increase in the sensitivity to T3 during the second trimester of fetal development. The main cellular targets of T3 appear to be the Cajal-Retzius and the subplate neurons. On the other hand, T3 regulates transcriptionally genes encoding extracellular matrix proteins, involved in cell migration and the control of diverse signaling pathways.

Changing patterns of synaptic input to subplate and cortical plate during development of visual cortex

1991 ◽  
Vol 66 (6) ◽  
pp. 2059-2071 ◽  
Author(s):  
E. Friauf ◽  
C. J. Shatz
Keyword(s):  
Cerebral Cortex ◽  
Visual Cortex ◽  
Synaptic Input ◽  
Field Potential ◽  
Short Latency ◽  
Cortical Plate ◽  
Synaptic Activation ◽  
Cortical Layers ◽  
Subplate Neurons ◽  
Monosynaptic Excitation

1. The development of excitatory activation in the visual cortex was studied in fetal and neonatal cats. During fetal and neonatal life, the immature cerebral cortex (the cortical plate) is sandwiched between two synaptic zones: the marginal zone above, and an area just below the cortical plate, the subplate. The subplate is transient and disappears by approximately 2 mo postnatal. Here we have investigated whether the subplate and the cortical plate receive functional synaptic inputs in the fetus, and when the adultlike pattern of excitatory synaptic input to the cortical plate appears during development. 2. Extracellular field potential recording to electrical stimulation of the optic radiation was performed in slices of cerebral cortex maintained in vitro. Laminar profiles of field potentials were converted by the current-source density (CSD) method to identify the spatial and temporal distribution of neuronal excitation within the subplate and the cortical plate. 3. Between embryonic day 47 (E47) and postnatal day 28 (P28; birth, E65), age-related changes occur in the pattern of synaptic activation of neurons in the cortical plate and the subplate. Early in development, at E47, E57, and P0, short-latency (probably monosynaptic) excitation is most obvious in the subplate, and longer latency (presumably polysynaptic) excitation can be seen in the cortical plate. Synaptic excitation in the subplate is no longer apparent at P21 and P28, a time when cell migration is finally complete and the cortical layers have formed. By contrast, excitation in the cortical plate is prominent in postnatal animals, and the temporal and spatial pattern has changed. 4. The adultlike sequence of synaptic activation in the different cortical layers can be seen by P28. It differs from earlier ages in several respects. First, short-latency (probably monosynaptic) excitation can be detected in cortical layer 4. Second, multisynaptic, long-lasting activation is present in layers 2/3 and 5. 5. Our results show that the subplate zone, known from anatomic studies to be a synaptic neurophil during development, receives functional excitatory inputs from axons that course in the developing white matter. Because the only mature neurons present in this zone are the subplate neurons, we conclude that subplate neurons are the principal, if not the exclusive, recipients of this input. The results suggest further that the excitation in the subplate in turn is relayed to neurons of the cortical plate via axon collaterals of subplate neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

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