Reelin-immunoreactive neurons in the adult vertebrate pallium

Pérez-García, Carlos G.; González-Delgado, F.J.; Suárez-Solá, M. Luisa; Castro-Fuentes, Rafael; Martin-Trujillo, Juan M.; Ferres-Torres, R; Meyer, Gundela

doi:10.1016/s0891-0618(00)00104-6

Cited by 60 publications

(79 citation statements)

References 49 publications

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“…The presence of reelin-expressing CR neurons in the outer layer of the developing pallium is evolutionarily conserved, and they have been reported in many amniote species, from turtles, crocodiles, lizards and rodents to primates, including human (Goffinet et al 1999;Perez-Garcia et al 2001;Molnar et al 2006). The increase in reelin levels in CR cells of the marginal zone has been suggested to be a driving factor in the progressive enlargement and differentiation of the pallium in evolution, with the highest reelin expression taking place in the human cortex (Tissir & Goffinet, 2003).…”

Section: The Importance Of Cajal-retzius Cells and Reelin For Corticamentioning

confidence: 99%

Building a human cortex: the evolutionary differentiation of Cajal‐Retzius cells and the cortical hem

Meyer

2010

Journal of Anatomy

102

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Cajal-Retzius (CR) cells are the most significant source of reelin, an extracellular matrix glycoprotein essential for cortical development. Strategically located in the marginal zone, CR cells control radial migration and laminar positioning of pyramidal neurons of the cortical plate. They degenerate and undergo cell death when cortical migration is completed. In human cortex development, reelin-expressing CR cells are already present in the early preplate, and continue to increase in number after the appearance of the cortical plate. In the course of the first half of gestation, the reelin signal in the marginal zone undergoes a huge amplification in parallel with the growth of the cortical plate and the expansion of the cortical surface. A significant source of CR cells is the cortical hem, a putative signalling centre at the interface of the prospective hippocampus and the choroid plexus. Hem-derived CR cells co-express reelin and p73, a transcription factor of the p53-family. They form the predominant CR cell population of the human neocortex. Characteristically, CR cells express the anti-apoptotic isoform DeltaNp73 which may be responsible for the protracted lifespan of human CR cells and the morphological differentiation of their axonal plexus. This dense fibre plexus, absent in lower mammals, amplifies the reelin-signal and establishes a physical boundary between the cortical plate and the marginal zone. In this review, we analyze the multiple sources of reelin ⁄ p73 positive CR cells at the interface of various telencephalic centres and the choroid plexus of the lateral ventricles. Additional populations of CR cells may derive from the thalamic eminence in the ventral thalamus and from the strionuclear neuroepithelium, or 'amygdalar hem'. Comparative studies in a variety of species indicate that the cortical hem is the main origin of CR cells destined for the neocortex, and is most highly developed in the human brain. The close association between cortical hem and choroid plexus suggests a concerted role in the evolutionary increase of CR cells, amplification of the reelin signal in the marginal zone, and cortical expansion.

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Section: The Importance Of Cajal-retzius Cells and Reelin For Corticamentioning

confidence: 99%

Building a human cortex: the evolutionary differentiation of Cajal‐Retzius cells and the cortical hem

Meyer

2010

Journal of Anatomy

102

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“…This primary antibody was previously used for visualizing reelin in the brain of numerous species belonging to all major classes of vertebrates from fishes to mammals (de Bergeyck et al 1998;Goffinet et al 1999;Smalheiser et al 2000;Perez-Garcia et al 2001;Martìnez-Cerdeño and Clascà 2002), including birds (Bernier et al 2000). Its specificity has been repeatedly demonstrated and is widely accepted (see references above).…”

Section: Reelin Immunocytochemistry-immunocytochemistrymentioning

confidence: 99%

Expression of reelin, its receptors and its intracellular signaling protein, Disabled1 in the canary brain: Relationships with the song control system

et al. 2008

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Songbirds produce learned vocalizations that are controlled by a specialized network of neural structures, the song control system. Several nuclei in this song control system demonstrate a marked degree of adult seasonal plasticity. Nucleus volume varies seasonally based on changes in cell size or spacing, and in the case of nucleus HVC and area X on the incorporation of new neurons. Reelin, a large glycoprotein defective in reeler mice, is assumed to determine the final location of migrating neurons in the developing brain. In mammals, reelin is also expressed in the adult brain but its functions are less well characterized. We investigated the relationships between the expression of reelin and/or its receptors and the dramatic seasonal plasticity in the canary (Serinus canaria) brain. We detected a broad distribution of the reelin protein, its messenger RNA and the mRNAs encoding for the reelin receptors (VLDLR and ApoER2) as well as for its intracellular signaling protein, Dab1. These different mRNAs and proteins did not display the same neuroanatomical distribution and were not clearly associated, in an exclusive manner, with telencephalic brain areas that incorporate new neurons in adulthood. Song control nuclei were associated with a particular specialized expression of reelin and its mRNA, with the reelin signal being either denser or lighter in the song nucleus than in the surrounding tissue. The density of reelin-ir structures did not seem to be affected by four weeks of treatment with exogenous testosterone. These observations do not provide conclusive evidence that reelin plays a prominent role in the positioning of new neurons in the adult canary brain but call for additional work on this protein analyzing its expression comparatively during development and in adulthood with a better temporal resolution at critical points in the reproductive cycle when brain plasticity is known to occur.

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“…The large projection cells of entorhinal layer II express Reelin (Drakew et al, 1998;Perez-Garcia et al, 2001) and define this area. In p73 ϩ/Ϫ mice, the entorhinal cortex was shifted into a more dorsal position, concurrent with an enlargement of the posterior cortical nucleus of the amygdala (Fig.…”

Section: The P73mentioning

confidence: 99%

Developmental Roles of p73 in Cajal-Retzius Cells and Cortical Patterning

Meyer¹,

Socorro²,

Garcia³

et al. 2004

J. Neurosci.

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122

129

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To examine the role of the p53 homolog p73 in brain development, we studied p73 Ϫ/Ϫ , p73 ϩ/Ϫ , E2F1 Ϫ/Ϫ , and reeler mutant mice. p73 in developing brain is expressed in Cajal-Retzius (CR) cells, the cortical hem, and the choroid plexus. p73-expressing CR cells are lost in p73 Ϫ/Ϫ embryos, although Reelin is faintly expressed in the marginal zone. Ectopic neurons in the p73 Ϫ/Ϫ preplate and cortical hem at embryonic day 12 implicate p73 in the early developmental program of the cortex; however, preplate partition and early cortical plate formation are not disturbed. Postnatal p73 Ϫ/Ϫ mice show a mild hypoplasia of the rostral cortex and a severely disrupted architecture of the posterior telencephalon. In the developing p73 Ϫ/Ϫ hippocampus, the most striking abnormality is the absence of the hippocampal fissure, suggesting a role of p73 in cortical folding. p73 ϩ/Ϫ mice have a less severe cortical phenotype; they display a dorsal shift of the entorhinal cortex and a reduced size of occipital and posterior temporal areas, which acquire entorhinal-like features such as Reelinpositive cells in layer II. CR cells appear unaffected by heterozygosity. We relate the malformations of the posterior pole in p73 mutant mice to alterations of p73 expression in the cortical hem and suggest that p73 forms part of an early signaling network that controls neocortical and archicortical regionalization. In mice deficient for the transcription factor E2F1, a main activator of the TAp73 (transactivating p73) isoform, we find a defect of the caudal cortical architecture resembling the p73 ϩ/Ϫ phenotype along with reduced TAp73 protein levels and propose that an E2F1-TAp73 dependent pathway is involved in cortical patterning.

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Reelin-immunoreactive neurons in the adult vertebrate pallium

Cited by 60 publications

References 49 publications

Building a human cortex: the evolutionary differentiation of Cajal‐Retzius cells and the cortical hem

Building a human cortex: the evolutionary differentiation of Cajal‐Retzius cells and the cortical hem

Expression of reelin, its receptors and its intracellular signaling protein, Disabled1 in the canary brain: Relationships with the song control system

Developmental Roles of p73 in Cajal-Retzius Cells and Cortical Patterning

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