ArticleCerebral cortex (New York, N.Y. : 1991)2013
Bilateral subcortical heterotopia with partial callosal agenesis in a mouse mutant.
Article in Cerebral cortex (New York, N.Y. : 1991), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
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- Cited2 Regulates Neocortical Layer II/III Generation and Somatosensory Callosal Projection Neuron Development and Connectivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Causes and consequences of gray matter heterotopia.CNS neuroscience & therapeutics · 2015Review
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- Gene co-regulation by Fezf2 selects neurotransmitter identity and connectivity of corticospinal neurons.Nature neuroscience · 2014Article
- Mutations in Eml1 lead to ectopic progenitors and neuronal heterotopia in mouse and human.Nature neuroscience · 2014Article
- Dampened hippocampal oscillations and enhanced spindle activity in an asymptomatic model of developmental cortical malformations.Frontiers in systems neuroscience · 2014Article
- Differential seizure response in two models of cortical heterotopia.Brain research · 2013Article
- A behavioral evaluation of sex differences in a mouse model of severe neuronal migration disorder.PloS one · 2013Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Cognition and behavior depend on the precise placement and interconnection of complex ensembles of neurons in cerebral cortex. Mutations that disrupt migration of immature neurons from the ventricular zone to the cortical plate have provided major insight into mechanisms of brain development and disease. We have discovered a new and highly penetrant spontaneous mutation that leads to large nodular bilateral subcortical heterotopias with partial callosal agenesis. The mutant phenotype was first detected in a colony of fully inbred BXD29 mice already known to harbor a mutation in Tlr4. Neurons confined to the heterotopias are mainly born in midgestation to late gestation and would normally have migrated into layers 2-4 of overlying neocortex. Callosal cross-sectional area and fiber number are reduced up to 50% compared with coisogenic wildtype BXD29 substrain controls. Mutants have a pronounced and highly selective defect in rapid auditory processing. The segregation pattern of the mutant phenotype is most consistent with a two-locus autosomal recessive model, and selective genotyping definitively rules out the Tlr4 mutation as a cause. The discovery of a novel mutation with strong pleiotropic anatomical and behavioral effects provides an important new resource for dissecting molecular mechanisms and functional consequences of errors of neuronal migration.
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