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1.
Kobe J Med Sci ; 58(3): E86-95, 2012 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-23143474

RESUMO

Subcortically projecting neurons and callosally projecting ones are distinct neuronal pools in the cerebral cortex of the rodents. However, cortical efferent neurons are known to project multiple targets transiently by plural collateral axons. These plural axons are eliminated during prenatal and postnatal development. In the cerebral cortex of the Reelin-deficient mouse, reeler, which is caused by mutation of the reelin gene, cortical efferent neurons are ectopically distributed. However, it is still unknown whether cortical efferent neurons in the reeler mouse lose surplus collateral axons or maintain them during developmental periods. If surplus collaterals of malpositioned cortical neurons are not eliminated, neurons projecting subcortically may project their axons to the contralateral hemisphere. To test this plausible hypothesis, we made double injections of two fluorescent dyes, Fast Blue and Diamidino yellow dihydrochloride into two of three regions, i.e., upper cervical cord, ventral lateral thalamic nucleus, and contralateral motor cortex of the normal and reeler mice, to label corticospinal, corticothalamic and callosal commissure neurons in the motor cortex, retrogradely. No double labeled neurons were identified in the motor cortex of the normal and reeler mice, although the distribution patterns of these cortical efferent neurons were completely different between normal and reeler mice. These findings strongly suggest that collateral elimination of cortical efferent neurons during developing periods are not affected in this mutant mouse.


Assuntos
Camundongos Mutantes Neurológicos , Córtex Motor/citologia , Neurônios/citologia , Medula Espinal/citologia , Amidinas , Animais , Feminino , Corantes Fluorescentes , Injeções , Masculino , Camundongos , Proteína Reelina , Tálamo
2.
Dev Dyn ; 236(9): 2694-701, 2007 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-17685489

RESUMO

Mouse genetic studies have identified several genes involved in cerebellar development. The mouse mutants staggerer and lurcher are functionally deficient for the retinoid-related orphan receptor alpha (ROR alpha) and glutamate receptor delta2 (Grid2) genes, respectively, and they show similar functional and developmental abnormalities in the cerebellum. Here, we report the cloning and expression pattern of zebrafish ROR alpha orthologues rora1 and rora2, and compare their expression pattern with that of grid2. Expression of rora1 and rora2 is initiated at late gastrula and pharyngula stages, respectively. Both rora1 and rora2 are spatially expressed in the retina and tectum. Expression of rora2 was further observed in the cerebellum, as reported for mammalian ROR alpha. In the adult brain, rora2 and grid2 are coexpressed in brain regions, designated as cerebellar-like structures. These observations suggest an evolutionarily conserved function of ROR alpha orthologues in the vertebrate brain.


Assuntos
Regulação da Expressão Gênica no Desenvolvimento , Receptores Citoplasmáticos e Nucleares/biossíntese , Proteínas de Peixe-Zebra/biossíntese , Sequência de Aminoácidos , Animais , Sequência de Bases , Cerebelo/embriologia , Clonagem Molecular , DNA Complementar/metabolismo , Éxons , Perfilação da Expressão Gênica , Dados de Sequência Molecular , Filogenia , Receptores de Glutamato/metabolismo , Homologia de Sequência de Aminoácidos , Peixe-Zebra
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