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of outstanding interest. Demonstrates that cerebellar granule cells express neuregulin (NRG) and that Bergman glia express the receptor tyrosine kinase erbB4. Antibody blockade of erbB4 blocks the conversion of cultured glial cells to a radial morphology that occurs when either neurons or NRG are added. In addition, dissociated radial glial cells expressing a dominant-negative erbB4 do not support the migration of cerebellar granule cells.
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Rio C, Rieff HI, Qi PM, Corfas G. Neuregulin and erbB receptors play a critical role in neuronal migration. of outstanding interest Neuron. 19:1997;39-50 Demonstrates that cerebellar granule cells express neuregulin (NRG) and that Bergman glia express the receptor tyrosine kinase erbB4. Antibody blockade of erbB4 blocks the conversion of cultured glial cells to a radial morphology that occurs when either neurons or NRG are added. In addition, dissociated radial glial cells expressing a dominant-negative erbB4 do not support the migration of cerebellar granule cells.
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Rio, C.1
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of outstanding interest. This paper used a neuregulin, glial growth factor 2 (GGF2), and function-blocking antibodies to demonstrate that GGF2 promotes migration of cortical neurons in elegant cortical imprint cultures and growth of radial glial processes. GGF2 is expressed by migrating neurons and cortical plate cells; a neuregulin receptor, erbB2, is expressed by radial glia, whereas neurons express erbB3 and erbB4. GGF2's effects may be mediated by a brain lipid-binding protein.
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Anton ES, Marchionni MA, Lee KF, Rakic P. Role of GGF/Neuregulin signaling in interactions between migrating neurons and radial glia in the developing cerebral cortex. of outstanding interest Development. 124:1997;3501-3510 This paper used a neuregulin, glial growth factor 2 (GGF2), and function-blocking antibodies to demonstrate that GGF2 promotes migration of cortical neurons in elegant cortical imprint cultures and growth of radial glial processes. GGF2 is expressed by migrating neurons and cortical plate cells; a neuregulin receptor, erbB2, is expressed by radial glia, whereas neurons express erbB3 and erbB4. GGF2's effects may be mediated by a brain lipid-binding protein.
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Anton, E.S.1
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CNS gene encoding astrotactin, which supports neuronal migration along glial fibers
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of outstanding interest. Molecular cloning of astrotactin (ASTN), a neuronal protein that functions in adhesion to glial cells, and, specifically, in neuronal locomotion of immature neurons along astroglial fibers. The gene encoding ASTN predicts a protein structure with three epidermal growth factor repeats and two fibronectin type III repeats. Astrotactin mRNA is expressed in postmitotic neurons undergoing migration in cortical regions of developing brain. Functional studies of the expressed protein demonstrate that antibodies against recombinant ASTN peptide block neuronal migration along glial fibers. This suggests that ASTN is a principal ligand for the directed migration of young neurons along the glial fiber system.
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Zheng C, Heintz N, Hatten ME. CNS gene encoding astrotactin, which supports neuronal migration along glial fibers. of outstanding interest Science. 272:1996;417-419 Molecular cloning of astrotactin (ASTN), a neuronal protein that functions in adhesion to glial cells, and, specifically, in neuronal locomotion of immature neurons along astroglial fibers. The gene encoding ASTN predicts a protein structure with three epidermal growth factor repeats and two fibronectin type III repeats. Astrotactin mRNA is expressed in postmitotic neurons undergoing migration in cortical regions of developing brain. Functional studies of the expressed protein demonstrate that antibodies against recombinant ASTN peptide block neuronal migration along glial fibers. This suggests that ASTN is a principal ligand for the directed migration of young neurons along the glial fiber system.
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The reeler gene encodes a protein with an EGF-like motif expressed by pioneer neurons
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Reelin is a secreted glycoprotein recognized by the CR-50 monoclonal antibody
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of special interest. A clear demonstration that reelin is secreted by COS cells expressing a full-length transcript, and by cerebellar explants. Also demonstrates that an epitope near the amino terminus of reelin is recognized by the CR-50 antibody, an important step in establishing the utility of this antibody.
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D'Arcangelo G, Nakajima K, Miyata T, Ogawa M, Mikoshiba K, Curran T. Reelin is a secreted glycoprotein recognized by the CR-50 monoclonal antibody. of special interest J Neurosci. 17:1997;23-31 A clear demonstration that reelin is secreted by COS cells expressing a full-length transcript, and by cerebellar explants. Also demonstrates that an epitope near the amino terminus of reelin is recognized by the CR-50 antibody, an important step in establishing the utility of this antibody.
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D'Arcangelo, G.1
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Curran, T.6
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30
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Reln(RI-Alb2), an allele of reeler isolated from a chlorambucil screen, is due to an IAP insertion with exon skipping
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Royaux I, Bernier B, Montgomery JC, Flaherty L, Goffinet AM. Reln(RI-Alb2), an allele of reeler isolated from a chlorambucil screen, is due to an IAP insertion with exon skipping. Genomics. 42:1997;479-482.
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Royaux, I.1
Bernier, B.2
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of outstanding interest. In a series of very difficult experiments, the authors demonstrate that late cortical neuronal progenitors continue to produce upper-layer neurons when transplanted into young cortex, where host progenitors are producing deeplayer neurons. Thus, although prior experiments had shown that early progenitors are capable of responding to environmental cues to produce upper-layer neurons when transplanted to late cortex, this study shows that late progenitors have lost the capability of producing deep-layer neurons.
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Frantz GD, McConnell SK. Restriction of late cerebral cortical progenitors to an upper-layer fate. of outstanding interest Neuron. 17:1996;55-61 In a series of very difficult experiments, the authors demonstrate that late cortical neuronal progenitors continue to produce upper-layer neurons when transplanted into young cortex, where host progenitors are producing deeplayer neurons. Thus, although prior experiments had shown that early progenitors are capable of responding to environmental cues to produce upper-layer neurons when transplanted to late cortex, this study shows that late progenitors have lost the capability of producing deep-layer neurons.
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McConnell, S.K.2
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Goffinet AM. A real gene for reeler. Nature. 374:1995;675-676.
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Disruption of hippocampal development in vivo by CR-50 mAb against reelin
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of special interest. An important demonstration that the CR-50 monoclonal antibody interferes with the function of reelin in vivo.
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Nakajima K, Mikoshiba K, Miyata T, Kudo C, Ogawa M. Disruption of hippocampal development in vivo by CR-50 mAb against reelin. of special interest Proc Natl Acad Sci USA. 94:1997;8196-8201 An important demonstration that the CR-50 monoclonal antibody interferes with the function of reelin in vivo.
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Proc Natl Acad Sci USA
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Nakajima, K.1
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Distribution of a reeler gene-related antigen in the developing cerebellum: An immunohistochemical study with an allogeneic antibody CR-50 on normal and reeler mice
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Miyata T, Nakajima K, Aruga J, Takahashi S, Ikenaka K, Mikoshiba K, Ogawa M. Distribution of a reeler gene-related antigen in the developing cerebellum: an immunohistochemical study with an allogeneic antibody CR-50 on normal and reeler mice. J Comp Neurol. 372:1996;215-228.
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44
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Regulation of Purkinje cell alignment by reelin as revealed with CR-50 antibody
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of special interest. An important step in the experimental analysis of reelin function, demonstrating that the reeler phenotype is replicated in cerebellar explant cultures by the CR-50 antibody and rescued, in part by reelin-producing cerebellar granule cells.
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Miyata T, Nakajima K, Mikoshiba K, Ogawa M. Regulation of Purkinje cell alignment by reelin as revealed with CR-50 antibody. of special interest J Neurosci. 17:1997;3599-3609 An important step in the experimental analysis of reelin function, demonstrating that the reeler phenotype is replicated in cerebellar explant cultures by the CR-50 antibody and rescued, in part by reelin-producing cerebellar granule cells.
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J Neurosci
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Miyata, T.1
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Ogawa, M.4
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45
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0030902291
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Cajal - Retzius cells regulate the radial glia phenotype in the adult and developing cerebellum and alter granule cell migration
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of special interest. A creative use of transgenic mice expressing markers for particular cell types, demonstrating that cells of the cortical marginal zone express a diffusible factor (not reelin) that causes mature cerebellar Bergman glia to express a juvenile phenotypic marker. Also demonstrates that immature Bergman glia extend processes into the marginal zone explant, and that cerebellar granule cells migrate into it, in the direction opposite their normal migration. Raises the intriguing prospect that cells of the marginal zone may produce a tropic factor for glial growth or neuronal migration.
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Soriano E, Alvarado-Mallart RM, Dumesnil N, Del Rio JA, Sotelo C. Cajal - Retzius cells regulate the radial glia phenotype in the adult and developing cerebellum and alter granule cell migration. of special interest Neuron. 18:1997;563-577 A creative use of transgenic mice expressing markers for particular cell types, demonstrating that cells of the cortical marginal zone express a diffusible factor (not reelin) that causes mature cerebellar Bergman glia to express a juvenile phenotypic marker. Also demonstrates that immature Bergman glia extend processes into the marginal zone explant, and that cerebellar granule cells migrate into it, in the direction opposite their normal migration. Raises the intriguing prospect that cells of the marginal zone may produce a tropic factor for glial growth or neuronal migration.
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Neuron
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Soriano, E.1
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Del Rio, J.A.4
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46
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A role for Cajal - Retzius cells and reelin in the development of hippocampal connections
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Del Rio JA, Heimrich B, Borrell V, Forster E, Drakew A, Alcantara S, Nakajima K, Miyata T, Ogawa M, Mikoshiba K, et al. A role for Cajal - Retzius cells and reelin in the development of hippocampal connections. Nature. 385:1997;70-74.
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Sweet HO, Bronson RT, Johnson KR, Cook SA, Davisson MT. Scrambler, a new neurological mutation of the mouse with abnormalities of neuronal migration. Mamm Genome. 7:1996;798-802.
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48
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0030719535
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A novel neurological mutation of mouse, yotari, which exhibits reeler-like phenotype but expresses reelin
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of special interest. Clear demonstration that a new mutation in mouse has the same cortical and cerebellar phenotype as reeler, but is not allelic to reelin and produces reelin. Also demonstrates that the defect is not attributable to an absence of cdk5, p35, or PAF-AH.
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Yonishema H, Nagata E, Matsumoto M, Yamada M, Nakajima K, Miyata T, Ogawa M, Mikoshiba K. A novel neurological mutation of mouse, yotari, which exhibits reeler-like phenotype but expresses reelin. of special interest Neurosci Res. 29:1997;217-223 Clear demonstration that a new mutation in mouse has the same cortical and cerebellar phenotype as reeler, but is not allelic to reelin and produces reelin. Also demonstrates that the defect is not attributable to an absence of cdk5, p35, or PAF-AH.
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Yonishema, H.1
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49
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of special interest. A careful analysis of neocortex and hippocampus in scrambler, demonstrating that both the morphology and the distribution of cell-birthdate cohorts are identical to reeler, thus suggesting that the scrambler gene product acts downstream of reeler
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Gonzalez JL, Goldowitz D, Sweet HO, Davisson MT, Walsh CA. Birthdate and cell marker analysis of scrambler: a novel mutation affecting cortical development with a reeler-like phenotype. of special interest J Neurosci. 17:1997;9204-9211 A careful analysis of neocortex and hippocampus in scrambler, demonstrating that both the morphology and the distribution of cell-birthdate cohorts are identical to reeler, thus suggesting that the scrambler gene product acts downstream of reeler.
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J Neurosci
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Gonzalez, J.L.1
Goldowitz, D.2
Sweet, H.O.3
Davisson, M.T.4
Walsh, C.A.5
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50
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0030831353
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Cerebellar disorganization characteristic of reeler in scrambler mutant mice despite presence of Reelin
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of special interest. A careful analysis of the cerebellum of scrambler, demonstrating that it is nearly identical to that of reeler, but that reelin is expressed normally, thus placing the action of the scrambler gene product either downstream of reelin or in an independent pathway.
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Goldowitz D, Cushing R, Laywell E, D'Arcangelo G, Sheldon M, Sweet H, Davisson M, Steindler D, Curran T. Cerebellar disorganization characteristic of reeler in scrambler mutant mice despite presence of Reelin. of special interest J Neurosci. 17:1997;8767-8777 A careful analysis of the cerebellum of scrambler, demonstrating that it is nearly identical to that of reeler, but that reelin is expressed normally, thus placing the action of the scrambler gene product either downstream of reelin or in an independent pathway.
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Goldowitz, D.1
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51
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0030704354
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Neuronal position in the developing brain is regulated by mouse disabled-1
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of outstanding interest. This paper demonstrates that targeted disruption of mdab1 produces the reeler phenotype, that the gene's protein product. mDab1 p80, is expressed in migrating cortical neurons, and that reelin is expressed normally in the knockout. The findings were critical in the identification of scrambler and yotari as alleles of mdab1 (see [52,53]).
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Howell BW, Hawkes R, Soriano P, Cooper JA. Neuronal position in the developing brain is regulated by mouse disabled-1. of outstanding interest Nature. 389:1997;733-737 This paper demonstrates that targeted disruption of mdab1 produces the reeler phenotype, that the gene's protein product. mDab1 p80, is expressed in migrating cortical neurons, and that reelin is expressed normally in the knockout. The findings were critical in the identification of scrambler and yotari as alleles of mdab1 (see [52,53]).
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Nature
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Howell, B.W.1
Hawkes, R.2
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Cooper, J.A.4
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52
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0030717493
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Scrambler and yotari disrupt the disabled gene and produce a reeler-like phenotype in mice
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of outstanding interest. Demonstrates that scrambler and yotari are alleles of mdab1, that both express mutant forms of mdab1 mRNA, and the mRNA is expressed in migrating cortical neurons that will come in contact with reelin. See also [51,53].
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Sheldon M, Rice DS, D'Arcangelo G, Yoneshima H, Nakajima K, Mikoshiba K, Howell BW, Cooper JA, Goldowitz D, Curran T. Scrambler and yotari disrupt the disabled gene and produce a reeler-like phenotype in mice. of outstanding interest Nature. 389:1997;730-733 Demonstrates that scrambler and yotari are alleles of mdab1, that both express mutant forms of mdab1 mRNA, and the mRNA is expressed in migrating cortical neurons that will come in contact with reelin. See also [51,53].
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Nature
, vol.389
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Sheldon, M.1
Rice, D.S.2
D'Arcangelo, G.3
Yoneshima, H.4
Nakajima, K.5
Mikoshiba, K.6
Howell, B.W.7
Cooper, J.A.8
Goldowitz, D.9
Curran, T.10
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53
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0030868450
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Aberrant splicing of a mouse disabled homolog, mdab1, in the scrambler mouse
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of outstanding interest. Demonstrates that mdab1 transcripts are abnormally spliced in scrambler, indicating that mdab1 is the scrambler gene. See also [51,52].
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Ware ML, Fox JW, Gonzalez JL, Davis NM, Derouvroit CL, Russo CJ, Chua SC, Goffinet AM, Walsh CA. Aberrant splicing of a mouse disabled homolog, mdab1, in the scrambler mouse. of outstanding interest Neuron. 19:1997;239-249 Demonstrates that mdab1 transcripts are abnormally spliced in scrambler, indicating that mdab1 is the scrambler gene. See also [51,52].
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Neuron
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Ware, M.L.1
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Gonzalez, J.L.3
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Howell BW, Gertler FB, Cooper JA. Mouse disabled (mDab1) - a Src binding protein implicated in neuronal development. EMBO J. 16:1997;121-132.
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55
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Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death
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of special interest. An important demonstration that targeted disruption of the gene for cyclin-dependent kinase 5 (cdk5) produces abnormal lamination of cerebral and cerebellar cortices.
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Ohshima T, Ward JM, Huh CG, Longenecker G, Veeranna Pant HC, Brady RO, Martin LJ, Kulkarni AB. Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death. of special interest Proc Natl Acad Sci USA. 93:1996;11173-11178 An important demonstration that targeted disruption of the gene for cyclin-dependent kinase 5 (cdk5) produces abnormal lamination of cerebral and cerebellar cortices.
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Ohshima, T.1
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Martin, L.J.7
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56
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0031018336
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Mice lacking p35, a neuronal specific activator of cdk5, display cortical lamination defects, seizures, and adult lethality
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of special interest. This paper reports that targeted disruption of p35, a neuron-specific activator of cdk5, produces abnormalities in cortical lamination, thus clearly implicating the cdk5/p35 complex in neuronal migration. The defects of mice lacking p35 are less severe than those lacking cdk5, suggesting that there may be other regulatory partners for cdk5.
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Chae T, Kwon YT, Bronson R, Dikkes P, Li E, Tsai LH. Mice lacking p35, a neuronal specific activator of cdk5, display cortical lamination defects, seizures, and adult lethality. of special interest Neuron. 18:1997;29-42 This paper reports that targeted disruption of p35, a neuron-specific activator of cdk5, produces abnormalities in cortical lamination, thus clearly implicating the cdk5/p35 complex in neuronal migration. The defects of mice lacking p35 are less severe than those lacking cdk5, suggesting that there may be other regulatory partners for cdk5.
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Neuron
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Chae, T.1
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A genetic animal model of human neocortical heterotopia associated with seizures
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Lee KS, Schottler F, Collins JL, Lanzino G, Couture D, Rao A, Hiramatsu K, Goto Y, Hong SC, Caner H, et al. A genetic animal model of human neocortical heterotopia associated with seizures. J Neurosci. 17:1997;6236-6242.
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Normam MG, McGillivray BC, Kalousek DK, Hill A, Poskitt KJ. Neuronal migration disorders and cortical dysplasias. Part I: migration disorders. Norman MG. Congenital Malformations of the Brain: Pathologic, Embryologic, Clinical, Radiologic and Genetic Aspects. 1995;223-277 Oxford University Press, New York.
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Dobyns WB, Truwit CL. Lissencephaly and other malformations of cortical development: 1995 update. Neuropediatrics. 26:1995;132-147.
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Isolation of a Miller-Dieker lissencephaly gene containing G protein beta-subunit-like repeats
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Targeted deletion of the pex2 peroxisome assembly gene in mice provides a model for Zellweger syndrome, a human neuronal migration disorder
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of outstanding interest. By using gene targeting in embryonic stem cells, the authors created a mouse model for Zellweger syndrome by deleting the gene encoding PEX2 peroxisomal integral membrane protein. These mice displayed intrauterine growth retardation, were severely hypotonic at birth and died within 12 hours. The mutant mice lack normal peroxisomes and display characteristic peroxisomal biochemical abnormalities. In the CNS of newborn mutant mice, there is disordered lamination in the cerebral cortex and an increased cell density in the underlying white matter, indicating an abnormality of neuronal migration. See also Baes et al. [72].
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of outstanding interest. By using gene targeting in embryonic stem cells, the authors created a mouse model for Zellweger syndrome by inactivating the PEX5 gene that encodes the PTS-1 import receptor for most peroxisomal proteins. These mice displayed intrauterine growth retardation, were severely hypotonic at birth and died within 72 hours. The mutant mice lacked normal peroxisomes and displayed characteristic peroxisomal biochemical abnormalities. Analysis of the neocortex revealed impaired neuronal migration and maturation, as well as extensive apoptotic death of neurons. See also Faust and Hatten [71].
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A nonmammalian homolog of the paf1 gene (Zellweger syndrome) discovered as a gene involved in caryogamy in the fungus podospora anserina
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Ross ME, Allen KM, Srivastava AK, Featherstone T, Gleeson JG, Hirsch B, Harding BN, Andermann E, Abdullah R, Berg M, et al. Linkage and physical mapping of X-linked lissencephaly/SBH (XLIS): a gene causing neuronal migration defects in human brain. of special interest Hum Mol Genet. 6:1997;555-562 X-linked lissencephaly and subcortical band heterotopia (SBH) are caused by mutation of a single gene. Using linkage analysis in five families, the XLIS gene has been mapped to Xq21-q24. The authors describe physical mapping of a balanced X ; 2 translocation (i.e., a translocation of chromosomal material between chromosomes 2 and X) in a girl with lissencephaly that further narrows the candidate genetic locus to Xq22.3-q23.
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Periventricular heterotopia - An X-linked dominant epilepsy locus causing aberrant cerebral cortical development
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of outstanding interest. This paper combines genetic mapping, magnetic resonance imaging, and pathologic analysis to define the epilepsy syndrome bilateral periventricular nodular heterotopia (BPNH) in four pedigrees. The authors identified a genetic locus at Xq28 that is linked to this disorder. Because of the presence of different neuronal types in different nodules, they suggest that the BPNH gene may be involved in proliferation of neuronal precursor cells, with loss of function resulting in formation of excessive numbers of cortical neurons that do not migrate properly.
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Eksioglu YZ, Scheffer IE, Cardenas P, Knoll J, Dimario F, Ramsby G, Berg M, Kamuro K, Berkovic SF, Duyk GM, et al. Periventricular heterotopia - an X-linked dominant epilepsy locus causing aberrant cerebral cortical development. of outstanding interest Neuron. 16:1996;77-87 This paper combines genetic mapping, magnetic resonance imaging, and pathologic analysis to define the epilepsy syndrome bilateral periventricular nodular heterotopia (BPNH) in four pedigrees. The authors identified a genetic locus at Xq28 that is linked to this disorder. Because of the presence of different neuronal types in different nodules, they suggest that the BPNH gene may be involved in proliferation of neuronal precursor cells, with loss of function resulting in formation of excessive numbers of cortical neurons that do not migrate properly.
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(1996)
Neuron
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Eksioglu, Y.Z.1
Scheffer, I.E.2
Cardenas, P.3
Knoll, J.4
Dimario, F.5
Ramsby, G.6
Berg, M.7
Kamuro, K.8
Berkovic, S.F.9
Duyk, G.M.10
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78
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0030826427
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Identification of a duplication of Xq28 associated with bilateral periventricular nodular heterotopia
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Fink JM, Dobyns WB, Guerrini R, Hirsch BA. Identification of a duplication of Xq28 associated with bilateral periventricular nodular heterotopia. Am J Hum Genet. 61:1997;379-387.
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Am J Hum Genet
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Fink, J.M.1
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Guerrini, R.3
Hirsch, B.A.4
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79
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Tangential migration of neurons in the developing cerebral cortex
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O'Rourke NA, Sullivan DP, Kaznowski CE, Jacobs AA, McConnell SK. Tangential migration of neurons in the developing cerebral cortex. Development. 121:1995;2165-2176.
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Development
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O'Rourke, N.A.1
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Kaznowski, C.E.3
Jacobs, A.A.4
McConnell, S.K.5
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80
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Expression of neuron-specific tubulin defines a novel population in the proliferative layers of the developing telencephalon
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Menezes JR, Luskin MB. Expression of neuron-specific tubulin defines a novel population in the proliferative layers of the developing telencephalon. J Neurosci. 14:1994;5399-5416.
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Menezes, J.R.1
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81
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Postmitotic neurons migrate tangentially in the cortical ventricular zone
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O'Rourke NA, Chenn A, McConnell SK. Postmitotic neurons migrate tangentially in the cortical ventricular zone. Development. 124:1997;997-1005.
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Development
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O'Rourke, N.A.1
Chenn, A.2
McConnell, S.K.3
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82
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Dispersion of neural progenitors within the germinal zones of the forebrain
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Fishell G, Mason CA, Hatten ME. Dispersion of neural progenitors within the germinal zones of the forebrain. Nature. 362:1993;636-638.
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Nature
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Fishell, G.1
Mason, C.A.2
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83
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Systematic widespread clonal organization in cerebral cortex
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Reid CB, Liang I, Walsh C. Systematic widespread clonal organization in cerebral cortex. Neuron. 15:1995;299-310.
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Neuron
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Reid, C.B.1
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Walsh, C.3
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84
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0027291286
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Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone
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Luskin MB. Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone. Neuron. 11:1993;173-189.
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Neuron
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Luskin, M.B.1
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85
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0030039879
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A comparison of the patterns of migration and the destinations of homotopically transplanted neonatal subventricular zone cells and heterotopically transplanted telencephalic ventricular zone cells
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Zigova T, Betarbet R, Soteres BJ, Brock S, Bakay RAE, Luskin MB. A comparison of the patterns of migration and the destinations of homotopically transplanted neonatal subventricular zone cells and heterotopically transplanted telencephalic ventricular zone cells. Dev Biol. 173:1996;459-474.
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Dev Biol
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Zigova, T.1
Betarbet, R.2
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Brock, S.4
Bakay, R.A.E.5
Luskin, M.B.6
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86
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A septum-derived chemorepulsive factor for migrating olfactory interneuron precursors
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Hu H, Rutishauser U. A septum-derived chemorepulsive factor for migrating olfactory interneuron precursors. Neuron. 16:1996;933-940.
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Neuron
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Hu, H.1
Rutishauser, U.2
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87
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The role of polysialic acid in migration of olfactory bulb interneuron precursors in the subventricular zone
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Hu H, Tomasiewics H, Magnuson T, Rutishauser U. The role of polysialic acid in migration of olfactory bulb interneuron precursors in the subventricular zone. Neuron. 16:1996;735-743.
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Neuron
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Hu, H.1
Tomasiewics, H.2
Magnuson, T.3
Rutishauser, U.4
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89
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0343051767
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Direct evidence for homotypic, glia-independent neuronal migration
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of outstanding interest. Demonstrates that migrating neurons from the SVZ use one another, not glia or accessory cells, as guides during postnatal migration into the olfactory bulb; this chain migration (see [88]) is characteristic of SVZ precursors and not precursors from neocortical VZ or cerebellar proliferative zones.
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Wichterle H, Garcia-Verdugo JM, Alvarez-Buylla A. Direct evidence for homotypic, glia-independent neuronal migration. of outstanding interest Neuron. 18:1997;779-791 Demonstrates that migrating neurons from the SVZ use one another, not glia or accessory cells, as guides during postnatal migration into the olfactory bulb; this chain migration (see [88]) is characteristic of SVZ precursors and not precursors from neocortical VZ or cerebellar proliferative zones.
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(1997)
Neuron
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Wichterle, H.1
Garcia-Verdugo, J.M.2
Alvarez-Buylla, A.3
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90
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Cellular composition and three-dimensional organization of the subventricular germinal zone in the adult mammalian brain
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Doetsch F, Garcia-Verdugo JM, Alvarez-Buylla A. Cellular composition and three-dimensional organization of the subventricular germinal zone in the adult mammalian brain. J Neurosci. 17:1997;5046-5061.
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J Neurosci
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Doetsch, F.1
Garcia-Verdugo, J.M.2
Alvarez-Buylla, A.3
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91
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0014990198
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Early prenatal ontogenesis of the cerebral cortex (neocortex) of the cat (Felis domestica). A Golgi study. I. The primordial neocortical organization
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Marin-Padilla M. Early prenatal ontogenesis of the cerebral cortex (neocortex) of the cat (Felis domestica). A Golgi study. I. The primordial neocortical organization. Z Anat Entwicklungsgesch. 134:1971;117-145.
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Marin-Padilla, M.1
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92
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Developmental changes in layer 1 of the human neocortex during prenatal life: A Diltracing and AchE and NADPH-d histochemistry study
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Meyer G, Gonzalez-Hernandez T. Developmental changes in layer 1 of the human neocortex during prenatal life: a Diltracing and AchE and NADPH-d histochemistry study. J Comp Neurol. 338:1993;317-336.
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93
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The human transient subpial granular layer: An optical, immunohistochemical, and ultrastructural analysis
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Gadisseux J-F, Goffinet AM, Lyon G, Evrard P. The human transient subpial granular layer: an optical, immunohistochemical, and ultrastructural analysis. J Comp Neurol. 324:1992;94-114.
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J Comp Neurol
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Gadisseux J-F1
Goffinet, A.M.2
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Evrard, P.4
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94
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Development and early postnatal maturation of the primary olfactory cortex
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Valverde F, Santacana M. Development and early postnatal maturation of the primary olfactory cortex. Dev Brain Res. 80:1994;96-114.
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Dev Brain Res
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Valverde, F.1
Santacana, M.2
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95
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0029787920
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Dynamics of cell migration from the lateral ganglionic eminence in the rat
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of outstanding interest. With difficult dye injections in whole-embryo cultures, the authors demonstrate that early-generated neurons from the LGE form the primary olfactory cortex. The paper also provides the first evidence that neurons cross the corticostriatal boundary from the LGE into the neocortical preplate.
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De Carlos JA, Lopez-Mascaraque L, Valverde F. Dynamics of cell migration from the lateral ganglionic eminence in the rat. of outstanding interest J Neurosci. 16:1996;6146-6156 With difficult dye injections in whole-embryo cultures, the authors demonstrate that early-generated neurons from the LGE form the primary olfactory cortex. The paper also provides the first evidence that neurons cross the corticostriatal boundary from the LGE into the neocortical preplate.
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(1996)
J Neurosci
, vol.16
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De Carlos, J.A.1
Lopez-Mascaraque, L.2
Valverde, F.3
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96
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0030698872
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Interneuron migration from basal forebrain to neocortex: Dependence on Dlx genes
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of outstanding interest. Demonstrates in organotypic slice-cultures that GABAergic neurons generated in the LGE migrate across the corticostriatal boundary into the MZ and IZ of the neocortex, and that this migration does not occur when both Dlx1 and Dlx2 are absent. This work directly challenges the notion that the neocortex arises solely from the neocortical VZ, and raises the intriguing possibility that the LGE supplies the majority of neocortical interneurons.
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Anderson SA, Eisenstat DD, Shi L, Rubenstein JLR. Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes. of outstanding interest Science. 278:1997;474-476 Demonstrates in organotypic slice-cultures that GABAergic neurons generated in the LGE migrate across the corticostriatal boundary into the MZ and IZ of the neocortex, and that this migration does not occur when both Dlx1 and Dlx2 are absent. This work directly challenges the notion that the neocortex arises solely from the neocortical VZ, and raises the intriguing possibility that the LGE supplies the majority of neocortical interneurons.
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(1997)
Science
, vol.278
, pp. 474-476
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Anderson, S.A.1
Eisenstat, D.D.2
Shi, L.3
Rubenstein, J.L.R.4
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97
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Cortical cells that migrate beyond area boundaries: Characterization of an early neuronal population in the lower intermediate zone of prenatal rats
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DeDiego I, Smith-Fernandez A, Fairen A. Cortical cells that migrate beyond area boundaries: characterization of an early neuronal population in the lower intermediate zone of prenatal rats. Eur J Neurosci. 6:1994;983-997.
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Eur J Neurosci
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Dediego, I.1
Smith-Fernandez, A.2
Fairen, A.3
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98
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0030862363
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Origin and route of tangentially migrating neurons in the developing neocortical intermediate zone
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of special interest. This paper demonstrates that the tangentially migrating neurons in the neocortical IZ are generated early and that, in vitro and in vivo, most of these neurons originate in the LGE.
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Tamamaki N, Fujimori KE, Takauji R. Origin and route of tangentially migrating neurons in the developing neocortical intermediate zone. of special interest J Neurosci. 17:1997;8313-8323 This paper demonstrates that the tangentially migrating neurons in the neocortical IZ are generated early and that, in vitro and in vivo, most of these neurons originate in the LGE.
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(1997)
J Neurosci
, vol.17
, pp. 8313-8323
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Tamamaki, N.1
Fujimori, K.E.2
Takauji, R.3
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99
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0030888786
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Neuronal heterotopias in the developing cerebral cortex produced by neurotrophin-4
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of outstanding interest. Demonstrates that exogenously applied NT4 induces a dramatic increase in the number of neurons in the neocortical MZ, both in organotypic slices and in vivo. NT4 does not rescue cortical neurons from cell death or cause them to proliferate, indicating that, in the presence of NT4, early-generated neurons migrate into the MZ from regions outside the neocortex
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Brunstrom JE, Gray-Swain MR, Osborne PA, Pearlman AL. Neuronal heterotopias in the developing cerebral cortex produced by neurotrophin-4. of outstanding interest Neuron. 18:1997;505-517 Demonstrates that exogenously applied NT4 induces a dramatic increase in the number of neurons in the neocortical MZ, both in organotypic slices and in vivo. NT4 does not rescue cortical neurons from cell death or cause them to proliferate, indicating that, in the presence of NT4, early-generated neurons migrate into the MZ from regions outside the neocortex.
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(1997)
Neuron
, vol.18
, pp. 505-517
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Brunstrom, J.E.1
Gray-Swain, M.R.2
Osborne, P.A.3
Pearlman, A.L.4
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