The hybrid reeler mouse.

J Hered

Published: March 1973

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http://dx.doi.org/10.1093/oxfordjournals.jhered.a108286DOI Listing

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In mammalian neocortex development, every cohort of newborn neurons is guided toward the marginal zone, leading to an "inside-out" organization of the 6 neocortical layers. This migratory pattern is regulated by the extracellular glycoprotein Reelin. The reeler mouse shows a homozygous mutation of the reelin gene.

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Reelin has fundamental functions in the developing and mature brain. Its absence gives rise to the Reeler phenotype in mice, the first described cerebellar mutation. In homozygous mutants missing the Reelin gene ( ), neurons are incapable of correctly positioning themselves in layered brain areas such as the cerebral and cerebellar cortices.

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The Reln gene encodes for the extracellular glycoprotein Reelin, which regulates several brain functions from development to adulthood, including neuronal migration, dendritic growth and branching and synapse formation and plasticity. Human studies have implicated Reelin signaling in several neurodevelopmental and psychiatric disorders. Mouse studies using the heterozygous Reeler (HR) mice have shown that reduced levels of Reln expression are associated with deficits in learning and memory and increased disinhibition.

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Departamento de Fisiología y Zoología, Universidad de Sevilla, c/o Profesor García González, no. 2, 41012, Sevilla, Spain.

We recently demonstrated that the mucosa of the small intestine of the rat expresses reelin and some components of its signaling system. The current study evaluates whether reelin affects the intestinal gene expression profile using microarray analysis and reeler mice, a natural mutant in which reelin is not expressed. The effect of the mutation on body weight and intestinal morphology is also evaluated.

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