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1.
Development ; 143(24): 4620-4630, 2016 12 15.
Artigo em Inglês | MEDLINE | ID: mdl-27965439

RESUMO

During forebrain development, radial glia generate neurons through the production of intermediate progenitor cells (IPCs). The production of IPCs is a central tenet underlying the generation of the appropriate number of cortical neurons, but the transcriptional logic underpinning this process remains poorly defined. Here, we examined IPC production using mice lacking the transcription factor nuclear factor I/X (Nfix). We show that Nfix deficiency delays IPC production and prolongs the neurogenic window, resulting in an increased number of neurons in the postnatal forebrain. Loss of additional Nfi alleles (Nfib) resulted in a severe delay in IPC generation while, conversely, overexpression of NFIX led to precocious IPC generation. Mechanistically, analyses of microarray and ChIP-seq datasets, coupled with the investigation of spindle orientation during radial glial cell division, revealed that NFIX promotes the generation of IPCs via the transcriptional upregulation of inscuteable (Insc). These data thereby provide novel insights into the mechanisms controlling the timely transition of radial glia into IPCs during forebrain development.


Assuntos
Proteínas de Ciclo Celular/biossíntese , Hipocampo/embriologia , Fatores de Transcrição NFI/genética , Células-Tronco Neurais/citologia , Neurogênese/genética , Animais , Proteínas de Ciclo Celular/genética , Regulação da Expressão Gênica , Camundongos , Camundongos Knockout , Neurogênese/fisiologia , Neurônios/citologia , Regiões Promotoras Genéticas/genética , Transcrição Gênica , Ativação Transcricional/genética
2.
Development ; 142(21): 3746-57, 2015 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-26534986

RESUMO

Transcription factors act during cortical development as master regulatory genes that specify cortical arealization and cellular identities. Although numerous transcription factors have been identified as being crucial for cortical development, little is known about their downstream targets and how they mediate the emergence of specific neuronal connections via selective axon guidance. The EMX transcription factors are essential for early patterning of the cerebral cortex, but whether EMX1 mediates interhemispheric connectivity by controlling corpus callosum formation remains unclear. Here, we demonstrate that in mice on the C57Bl/6 background EMX1 plays an essential role in the midline crossing of an axonal subpopulation of the corpus callosum derived from the anterior cingulate cortex. In the absence of EMX1, cingulate axons display reduced expression of the axon guidance receptor NRP1 and form aberrant axonal bundles within the rostral corpus callosum. EMX1 also functions as a transcriptional activator of Nrp1 expression in vitro, and overexpression of this protein in Emx1 knockout mice rescues the midline-crossing phenotype. These findings reveal a novel role for the EMX1 transcription factor in establishing cortical connectivity by regulating the interhemispheric wiring of a subpopulation of neurons within the mouse anterior cingulate cortex.


Assuntos
Giro do Cíngulo/metabolismo , Proteínas de Homeodomínio/metabolismo , Neuropilina-1/metabolismo , Fatores de Transcrição/metabolismo , Agenesia do Corpo Caloso/embriologia , Agenesia do Corpo Caloso/genética , Animais , Axônios/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Knockout , Semaforinas/metabolismo
4.
Cereb Cortex ; 25(7): 1970-80, 2015 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24518754

RESUMO

Cortical development in the mouse embryo involves complex changes in the microstructure of the telencephalic wall, which are challenging to examine using three-dimensional (3D) imaging techniques. In this study, high-resolution 3D diffusion magnetic resonance (dMR) microscopy of the embryonic mouse cortex is presented. Using diffusion-weighted gradient- and spin-echo based acquisition, dMR microimaging data were acquired from fixed mouse embryos at 7 developmental stages from embryonic day (E)12.5 to E18.5. The dMR imaging (dMRI) contrasts revealed microscopic structural detail in the mouse telencephalic wall, allowing delineation of transient zones in the developing cortex based on their unique diffusion signatures. With the high-resolution 3D data of the mouse embryo, we were able to visualize the complex microstructure of embryonic cerebral tissue and to resolve its regional and temporal evolution during cortical formation. Furthermore, averaged dMRI contrasts generated via deformable registration revealed distinct spatial and temporal gradients of anisotropy variation across the developing embryonic cortical plate and the ventricular zone. The findings of this study demonstrate the potential of 3D dMRI to resolve the complex microstructure of the embryonic mouse cortex, and will be important for investigations of corticogenesis and its disruption in embryonic mouse models.


Assuntos
Córtex Cerebral/embriologia , Imagem de Difusão por Ressonância Magnética/métodos , Microscopia/métodos , Animais , Anisotropia , Imunofluorescência , Imageamento Tridimensional , Camundongos Endogâmicos C57BL , Organogênese
5.
Dev Biol ; 365(1): 36-49, 2012 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-22349628

RESUMO

The Slit molecules are chemorepulsive ligands that regulate axon guidance at the midline of both vertebrates and invertebrates. In mammals, there are three Slit genes, but only Slit2 has been studied in any detail with regard to mammalian brain commissure formation. Here, we sought to understand the relative contributions that Slit proteins make to the formation of the largest brain commissure, the corpus callosum. Slit ligands bind Robo receptors, and previous studies have shown that Robo1(-/-) mice have defects in corpus callosum development. However, whether the Slit genes signal exclusively through Robo1 during callosal formation is unclear. To investigate this, we compared the development of the corpus callosum in both Slit2(-/-) and Robo1(-/-) mice using diffusion magnetic resonance imaging. This analysis demonstrated similarities in the phenotypes of these mice, but crucially also highlighted subtle differences, particularly with regard to the guidance of post-crossing axons. Analysis of single mutations in Slit family members revealed corpus callosum defects (but not complete agenesis) in 100% of Slit2(-/-) mice and 30% of Slit3(-/-) mice, whereas 100% of Slit1(-/-); Slit2(-/-) mice displayed complete agenesis of the corpus callosum. These results revealed a role for Slit1 in corpus callosum development, and demonstrated that Slit2 was necessary but not sufficient for midline crossing in vivo. However, co-culture experiments utilising Robo1(-/-) tissue versus Slit2 expressing cell blocks demonstrated that Slit2 was sufficient for the guidance activity mediated by Robo1 in pre-crossing neocortical axons. This suggested that Slit1 and Slit3 might also be involved in regulating other mechanisms that allow the corpus callosum to form, such as the establishment of midline glial populations. Investigation of this revealed defects in the development and dorso-ventral positioning of the indusium griseum glia in multiple Slit mutants. These findings indicate that Slits regulate callosal development via both classical chemorepulsive mechanisms, and via a novel role in mediating the correct positioning of midline glial populations. Finally, our data also indicate that some of the roles of Slit proteins at the midline may be independent of Robo signalling, suggestive of additional receptors regulating Slit signalling during development.


Assuntos
Corpo Caloso/embriologia , Peptídeos e Proteínas de Sinalização Intercelular/fisiologia , Proteínas do Tecido Nervoso/fisiologia , Animais , Diferenciação Celular , Técnicas de Cocultura , Corpo Caloso/citologia , Corpo Caloso/fisiologia , Regulação da Expressão Gênica no Desenvolvimento , Peptídeos e Proteínas de Sinalização Intercelular/genética , Imageamento por Ressonância Magnética , Proteínas de Membrana/genética , Proteínas de Membrana/fisiologia , Camundongos , Proteínas do Tecido Nervoso/genética , Neuroglia/citologia , Neuroglia/fisiologia , Receptores Imunológicos/genética , Receptores Imunológicos/fisiologia , Transdução de Sinais , Proteínas Roundabout
6.
Elife ; 102021 05 04.
Artigo em Inglês | MEDLINE | ID: mdl-33945466

RESUMO

Corpus callosum dysgenesis (CCD) is a congenital disorder that incorporates either partial or complete absence of the largest cerebral commissure. Remodelling of the interhemispheric fissure (IHF) provides a substrate for callosal axons to cross between hemispheres, and its failure is the main cause of complete CCD. However, it is unclear whether defects in this process could give rise to the heterogeneity of expressivity and phenotypes seen in human cases of CCD. We identify incomplete IHF remodelling as the key structural correlate for the range of callosal abnormalities in inbred and outcrossed BTBR mouse strains, as well as in humans with partial CCD. We identify an eight base-pair deletion in Draxin and misregulated astroglial and leptomeningeal proliferation as genetic and cellular factors for variable IHF remodelling and CCD in BTBR strains. These findings support a model where genetic events determine corpus callosum structure by influencing leptomeningeal-astroglial interactions at the IHF.


Assuntos
Agenesia do Corpo Caloso/genética , Corpo Caloso/fisiologia , Regulação da Expressão Gênica no Desenvolvimento/genética , Peptídeos e Proteínas de Sinalização Intercelular/genética , Adulto , Idoso , Agenesia do Corpo Caloso/patologia , Animais , Estudos de Coortes , Corpo Caloso/crescimento & desenvolvimento , Corpo Caloso/patologia , Feminino , Células HEK293 , Humanos , Masculino , Camundongos , Pessoa de Meia-Idade , Fenótipo , Adulto Jovem
7.
Elife ; 102021 04 19.
Artigo em Inglês | MEDLINE | ID: mdl-33871356

RESUMO

The forebrain hemispheres are predominantly separated during embryogenesis by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form a continuous substrate between the hemispheres for midline crossing of the corpus callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma (DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved function in commissural axon guidance. The CC and HC are absent in Dcc and Ntn1 knockout mice, while other commissures are only partially affected, suggesting an additional aetiology in forebrain commissure formation. Here, we find that these molecules play a critical role in regulating astroglial development and IHF remodelling during CC and HC formation. Human subjects with DCC mutations display disrupted IHF remodelling associated with CC and HC malformations. Thus, axon guidance molecules such as DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures prior to their role in regulating axonal growth and guidance across it.


Assuntos
Astrócitos/metabolismo , Corpo Caloso/metabolismo , Receptor DCC/metabolismo , Telencéfalo/metabolismo , Agenesia do Corpo Caloso/genética , Agenesia do Corpo Caloso/metabolismo , Agenesia do Corpo Caloso/patologia , Animais , Células COS , Linhagem Celular Tumoral , Movimento Celular , Forma Celular , Chlorocebus aethiops , Corpo Caloso/embriologia , Receptor DCC/genética , Regulação da Expressão Gênica no Desenvolvimento , Genótipo , Idade Gestacional , Células HEK293 , Humanos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Morfogênese , Mutação , Netrina-1/genética , Netrina-1/metabolismo , Fenótipo , Transdução de Sinais , Telencéfalo/embriologia
8.
Semin Hematol ; 57(4): 194-200, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33256912

RESUMO

Natural killer (NK) cells are an important component of the innate immune system, particularly for metastasis immunosurveillance. They can rapidly recognize and kill transformed cells without the requirement of specific neo-antigen recognition. Their effector functions are modulated by a range of stimulatory and inhibitory surface receptors that regulate their cellular activation, differentiation and homeostasis. However, cancer cells can evade NK cell detection by receptor interaction or secretion of soluble immunosuppressant molecules. Therefore, genetic reprogramming of these immune suppressing or activating receptors of NK cells is a promising strategy to augment NK cell tumoricidal functions. In this review, we highlight the current clinical trials of chimeric antigen receptor engineered NK cells with redirected antigen specificity to eliminate hematological cancers and solid tumors. New alternative strategies that are advancing NK cell engineering for cancer treatment are also outlined. Lastly, different NK cell transgenesis approaches are reviewed and compared, and we discuss how these methods can be employed to maximize their anti-tumor effector functions.


Assuntos
Imunoterapia/métodos , Células Matadoras Naturais/imunologia , Neoplasias/terapia , Humanos , Neoplasias/imunologia
9.
Nat Commun ; 9(1): 306, 2018 01 22.
Artigo em Inglês | MEDLINE | ID: mdl-29358753

RESUMO

Mounting evidence suggests that neuronal activity influences myelination, potentially allowing for experience-driven modulation of neural circuitry. The degree to which neuronal activity is capable of regulating myelination at the individual axon level is unclear. Here we demonstrate that stimulation of somatosensory axons in the mouse brain increases proliferation and differentiation of oligodendrocyte progenitor cells (OPCs) within the underlying white matter. Stimulated axons display an increased probability of being myelinated compared to neighboring non-stimulated axons, in addition to being ensheathed with thicker myelin. Conversely, attenuating neuronal firing reduces axonal myelination in a selective activity-dependent manner. Our findings reveal that the process of selecting axons for myelination is strongly influenced by the relative activity of individual axons within a population. These observed cellular changes are consistent with the emerging concept that adaptive myelination is a key mechanism for the fine-tuning of neuronal circuitry in the mammalian CNS.


Assuntos
Axônios/metabolismo , Encéfalo/metabolismo , Bainha de Mielina/metabolismo , Fibras Nervosas Mielinizadas/metabolismo , Células-Tronco Neurais/citologia , Animais , Encéfalo/citologia , Encéfalo/crescimento & desenvolvimento , Diferenciação Celular , Proliferação de Células , Clozapina/farmacologia , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Oligodendroglia/citologia
10.
Neural Dev ; 12(1): 9, 2017 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-28558801

RESUMO

The corpus callosum forms the major interhemispheric connection in the human brain and is unique to eutherian (or placental) mammals. The developmental events associated with the evolutionary emergence of this structure, however, remain poorly understood. A key step in callosal formation is the prior remodeling of the interhemispheric fissure by embryonic astroglial cells, which then subsequently act as a permissive substrate for callosal axons, enabling them to cross the interhemispheric midline. However, whether astroglial-mediated interhemispheric remodeling is unique to eutherian mammals, and thus possibly associated with the phylogenetic origin of the corpus callosum, or instead is a general feature of mammalian brain development, is not yet known. To investigate this, we performed a comparative analysis of interhemispheric remodeling in eutherian and non-eutherian mammals, whose lineages branched off before the evolution of the corpus callosum. Whole brain MRI analyses revealed that the interhemispheric fissure is retained into adulthood in marsupials and monotremes, in contrast to eutherians (mice), in which the fissure is significantly remodeled throughout development. Histological analyses further demonstrated that, while midline astroglia are present in developing marsupials, these cells do not intercalate with one another through the intervening interhemispheric fissure, as they do in developing mice. Thus, developing marsupials do not undergo astroglial-mediated interhemispheric remodeling. As remodeling of the interhemispheric fissure is essential for the subsequent formation of the corpus callosum in eutherians, our data highlight the role of astroglial-mediated interhemispheric remodeling in the evolutionary origin of the corpus callosum.


Assuntos
Astrócitos/fisiologia , Corpo Caloso/crescimento & desenvolvimento , Eutérios/crescimento & desenvolvimento , Telencéfalo/crescimento & desenvolvimento , Animais , Evolução Biológica , Corpo Caloso/anatomia & histologia , Eutérios/anatomia & histologia , Especificidade da Espécie
11.
Nat Genet ; 49(4): 511-514, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28250454

RESUMO

Brain malformations involving the corpus callosum are common in children with developmental disabilities. We identified DCC mutations in four families and five sporadic individuals with isolated agenesis of the corpus callosum (ACC) without intellectual disability. DCC mutations result in variable dominant phenotypes with decreased penetrance, including mirror movements and ACC associated with a favorable developmental prognosis. Possible phenotypic modifiers include the type and location of mutation and the sex of the individual.


Assuntos
Agenesia do Corpo Caloso/genética , Deficiências do Desenvolvimento/genética , Mutação/genética , Receptores de Superfície Celular/genética , Proteínas Supressoras de Tumor/genética , Anormalidades Múltiplas/genética , Encéfalo/patologia , Corpo Caloso/patologia , Receptor DCC , Família , Feminino , Humanos , Masculino , Malformações do Sistema Nervoso/genética , Células-Tronco Neurais/patologia , Penetrância , Fenótipo
12.
Cell Rep ; 17(3): 735-747, 2016 10 11.
Artigo em Inglês | MEDLINE | ID: mdl-27732850

RESUMO

The corpus callosum is the major axon tract that connects and integrates neural activity between the two cerebral hemispheres. Although ∼1:4,000 children are born with developmental absence of the corpus callosum, the primary etiology of this condition remains unknown. Here, we demonstrate that midline crossing of callosal axons is dependent upon the prior remodeling and degradation of the intervening interhemispheric fissure. This remodeling event is initiated by astroglia on either side of the interhemispheric fissure, which intercalate with one another and degrade the intervening leptomeninges. Callosal axons then preferentially extend over these specialized astroglial cells to cross the midline. A key regulatory step in interhemispheric remodeling is the differentiation of these astroglia from radial glia, which is initiated by Fgf8 signaling to downstream Nfi transcription factors. Crucially, our findings from human neuroimaging studies reveal that developmental defects in interhemispheric remodeling are likely to be a primary etiology underlying human callosal agenesis.


Assuntos
Astrócitos/metabolismo , Cérebro/embriologia , Corpo Caloso/embriologia , Organogênese , Agenesia do Corpo Caloso/genética , Agenesia do Corpo Caloso/patologia , Animais , Axônios/metabolismo , Diferenciação Celular , Corpo Caloso/metabolismo , Corpo Caloso/patologia , Fator 8 de Crescimento de Fibroblasto/metabolismo , Humanos , Camundongos , Fenótipo , Transdução de Sinais , Fatores de Transcrição/metabolismo
13.
Neural Dev ; 10: 10, 2015 Apr 03.
Artigo em Inglês | MEDLINE | ID: mdl-25879444

RESUMO

BACKGROUND: Autism spectrum disorders (ASD) are a group of poorly understood behavioural disorders, which have increased in prevalence in the past two decades. Animal models offer the opportunity to understand the biological basis of these disorders. Studies comparing different mouse strains have identified the inbred BTBR T + tf/J (BTBR) strain as a mouse model of ASD based on its anti-social and repetitive behaviours. Adult BTBR mice have complete agenesis of the corpus callosum, reduced cortical thickness and changes in early neurogenesis. However, little is known about the development or ultimate organisation of cortical areas devoted to specific sensory and motor functions in these mice that may also contribute to their behavioural phenotype. RESULTS: In this study, we performed diffusion tensor imaging and tractography, together with histological analyses to investigate the emergence of functional areas in the cerebral cortex and their connections in BTBR mice and age-matched C57Bl/6 control mice. We found evidence that neither the anterior commissure nor the hippocampal commissure compensate for the loss of callosal connections, indicating that no interhemispheric neocortical connectivity is present in BTBR mice. We also found that both the primary visual and somatosensory cortical areas are shifted medially in BTBR mice compared to controls and that cortical thickness is differentially altered in BTBR mice between cortical areas and throughout development. CONCLUSIONS: We demonstrate that interhemispheric connectivity and cortical area formation are altered in an age- and region-specific manner in BTBR mice, which may contribute to the behavioural deficits previously observed in this strain. Some of these developmental patterns of change are also present in human ASD patients, and elucidating the aetiology driving cortical changes in BTBR mice may therefore help to increase our understanding of this disorder.


Assuntos
Transtorno do Espectro Autista/patologia , Córtex Cerebral/patologia , Agenesia do Corpo Caloso/genética , Agenesia do Corpo Caloso/patologia , Envelhecimento/patologia , Animais , Comissura Anterior/patologia , Imagem de Tensor de Difusão , Modelos Animais de Doenças , Fórnice/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos , Camundongos Mutantes Neurológicos , Fenótipo , Córtex Somatossensorial/patologia , Córtex Visual/patologia
14.
Front Hum Neurosci ; 8: 497, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25071525

RESUMO

Axonal connections between the left and right sides of the brain are crucial for bilateral integration of lateralized sensory, motor, and associative functions. Throughout vertebrate species, forebrain commissures share a conserved developmental plan, a similar position relative to each other within the brain and similar patterns of connectivity. However, major events in the evolution of the vertebrate brain, such as the expansion of the telencephalon in tetrapods and the origin of the six-layered isocortex in mammals, resulted in the emergence and diversification of new commissural routes. These new interhemispheric connections include the pallial commissure, which appeared in the ancestors of tetrapods and connects the left and right sides of the medial pallium (hippocampus in mammals), and the corpus callosum, which is exclusive to eutherian (placental) mammals and connects both isocortical hemispheres. A comparative analysis of commissural systems in vertebrates reveals that the emergence of new commissural routes may have involved co-option of developmental mechanisms and anatomical substrates of preexistent commissural pathways. One of the embryonic regions of interest for studying these processes is the commissural plate, a portion of the early telencephalic midline that provides molecular specification and a cellular scaffold for the development of commissural axons. Further investigations into these embryonic processes in carefully selected species will provide insights not only into the mechanisms driving commissural evolution, but also regarding more general biological problems such as the role of developmental plasticity in evolutionary change.

15.
Mol Autism ; 5: 57, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25874073

RESUMO

BACKGROUND: There is converging preclinical and clinical evidence to suggest that the extracellular signal-regulated kinase (ERK) signaling pathway may be dysregulated in autism spectrum disorders. METHOD: We evaluated Mapk/Erk1/2, cellular proliferation and apoptosis in BTBR mice, as a preclinical model of Autism. We had previously generated 410 F2 mice from the cross of BTBR with B6. At that time, six different social behaviors in all F2 mice were evaluated and scored. In this study, eight mice at each extreme of the social behavioral spectrum were selected and the expression and activity levels of Mapk/Erk in the prefrontal cortex and cerebellum of these mice were compared. Finally, we compared the Mapk/Erk signaling pathway in brain and lymphocytes of the same mice, testing for correlation in the degree of kinase activation across these separate tissues. RESULTS: Levels of phosphorylated Erk (p-Erk) were significantly increased in the brains of BTBR versus control mice. We also observed a significant association between juvenile social behavior and phosphorylated mitogen-activated protein kinase kinase (p-Mek) and p-Erk levels in the prefrontal cortex but not in the cerebellum. In contrast, we did not find a significant association between social behavior and total protein levels of either Mek or Erk. We also tested whether steady-state levels of Erk activation in the cerebral cortex in individual animals correlated with levels of Erk activation in lymphocytes, finding a significant relationship for this signaling pathway. CONCLUSION: These observations suggest that dysregulation of the ERK signaling pathway may be an important mediator of social behavior, and that measuring activation of this pathway in peripheral lymphocytes may serve as a surrogate marker for central nervous system (CNS) ERK activity, and possibly autistic behavior.

16.
J Comp Neurol ; 518(18): 3645-61, 2010 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-20653027

RESUMO

Coordinated transfer of information between the brain hemispheres is essential for function and occurs via three axonal commissures in the telencephalon: the corpus callosum (CC), hippocampal commissure (HC), and anterior commissure (AC). Commissural malformations occur in over 50 human congenital syndromes causing mild to severe cognitive impairment. Disruption of multiple commissures in some syndromes suggests that common mechanisms may underpin their development. Diffusion tensor magnetic resonance imaging revealed that forebrain commissures crossed the midline in a highly specific manner within an oblique plane of tissue, referred to as the commissural plate. This specific anatomical positioning suggests that correct patterning of the commissural plate may influence forebrain commissure formation. No analysis of the molecular specification of the commissural plate has been performed in any species; therefore, we utilized specific transcription factor markers to delineate the commissural plate and identify its various subdomains. We found that the mouse commissural plate consists of four domains and tested the hypothesis that disruption of these domains might affect commissure formation. Disruption of the dorsal domains occurred in strains with commissural defects such as Emx2 and Nfia knockout mice but commissural plate patterning was normal in other acallosal strains such as Satb2(-/-). Finally, we demonstrate an essential role for the morphogen Fgf8 in establishing the commissural plate at later developmental stages. The results demonstrate that correct patterning of the commissural plate is an important mechanism in forebrain commissure formation.


Assuntos
Telencéfalo/anormalidades , Telencéfalo/anatomia & histologia , Telencéfalo/embriologia , Animais , Imagem de Tensor de Difusão , Fator 8 de Crescimento de Fibroblasto/genética , Fator 8 de Crescimento de Fibroblasto/metabolismo , Proteínas de Homeodomínio/genética , Humanos , Imuno-Histoquímica , Proteínas de Ligação à Região de Interação com a Matriz/genética , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fatores de Transcrição NFI/genética , Telencéfalo/metabolismo , Fatores de Transcrição/genética
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