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Cerebral Cortex Advance Access published online on July 26, 2007
Cerebral Cortex, doi:10.1093/cercor/bhm132
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© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Absence of LPA1 Signaling Results in Defective Cortical Development

Guillermo Estivill-Torrús1, Pedro Llebrez-Zayas1, Elisa Matas-Rico1, Luis Santín2, Carmen Pedraza2, Isabel De Diego3, Ignacio Del Arco1, Pedro Fernández-Llebrez4, Jerold Chun5 and Fernando Rodríguez De Fonseca1

1 Unidad de Investigación, Fundación IMABIS, Hospital Carlos Haya, E-29010 Málaga, Spain, 2 Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Facultad de Psicología, Universidad de Málaga, Campus de Teatinos, E-29071, Málaga, Spain, 3 Departamento de Anatomía y Medicina Legal, Facultad de Medicina, Universidad de Málaga, Campus de Teatinos, E-29071, Málaga, Spain, 4 Departamento de Biología Celular, Genética y Fisiología, Facultad de Ciencias, Universidad de Málaga, Campus de Teatinos, E-29071, Málaga, Spain, 5 Department of Molecular Biology, Helen L. Dorris Child and Adolescent Neuropsychiatric Disorder Institute, The Scripps Research Institute, La Jolla, CA 92037, USA

Address correspondence to Guillermo Estivill-Torrús, Unidad de Investigación, Fundación IMABIS, Hospital Carlos Haya, Pabellón A, planta 7a, Avenida Carlos Haya 82, E-29010 Málaga, Spain. Email: guillermo.estivill{at}fundacionimabis.org.

Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein–coupled receptors. At least 2 LPA receptors, LPA1 and LPA2, are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA1 loss-of-function mutants reported did not show gross cerebral cortical defects in the 50% that survived perinatal demise. Here, we report a role for LPA1 in cortical neural precursors resulting from analysis of a variant of a previously characterized LPA1-null mutant that arose spontaneously during colony expansion. These LPA1-null mice, termed maLPA1, exhibit almost complete perinatal viability and show a reduced VZ, altered neuronal markers, and increased cortical cell death that results in a loss of cortical layer cellularity in adults. These data support LPA1 function in normal cortical development and suggest that the presence of genetic modifiers of LPA1 influences cerebral cortical development.

Key Words: brain development • cerebral cortex • LPA • lysophosphatidic acid • neurogenesis


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