ArticleThe American journal of pathology2004
Lis1 is necessary for normal non-radial migration of inhibitory interneurons.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- The Role of Hippocampal Interneuron Migration in Neurodevelopmental Disorders: A Systematic Review.Hippocampus · 2026Pooled it
- When the Cytoskeleton Fails: Primary Structural Defects Underlying Disorders with Neurological Involvement.International journal of molecular sciences · 2026Review
- Selective Lis1 inactivation disrupts migration and positioning of cortical somatostatin interneurons.Scientific reports · 2026Article
- Cortical Parvalbumin-Positive Interneuron Development and Function Are Altered in the APC Conditional Knockout Mouse Model of Infantile and Epileptic Spasms Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Interneuron odyssey: molecular mechanisms of tangential migration.Frontiers in neural circuits · 2023Review
- Abnormalities in Cortical GABAergic Interneurons of the Primary Motor Cortex Caused byFrontiers in cell and developmental biology · 2022Article
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- Article
- More Than Mortar: Glia as Architects of Nervous System Development and Disease.Frontiers in cell and developmental biology · 2020Review
- Ex Utero Electroporation and Organotypic Slice Cultures of Embryonic Mouse Brains for Live-Imaging of Migrating GABAergic Interneurons.Journal of visualized experiments : JoVE · 2018Article
- INTERNEURONOPATHIES AND THEIR ROLE IN EARLY LIFE EPILEPSIES AND NEURODEVELOPMENTAL DISORDERS.Epilepsia open · 2017Article
- PAFAH1B1 haploinsufficiency disrupts GABA neurons and synaptic E/I balance in the dentate gyrus.Scientific reports · 2017Article
- Elongator controls cortical interneuron migration by regulating actomyosin dynamics.Cell research · 2016Article
- Neuronal migration disorders: Focus on the cytoskeleton and epilepsy.Neurobiology of disease · 2016Review
- Early rescue of interneuron disease trajectory in developmental epilepsies.Current opinion in neurobiology · 2016Review
- Crosstalk between intracellular and extracellular signals regulating interneuron production, migration and integration into the cortex.Frontiers in cellular neuroscience · 2015Review
- SDF1 reduces interneuron leading process branching through dual regulation of actin and microtubules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- DISC1 knockdown impairs the tangential migration of cortical interneurons by affecting the actin cytoskeleton.Frontiers in cellular neuroscience · 2014Article
- Using the neurofibromatosis tumor predisposition syndromes to understand normal nervous system development.Scientifica · 2014Review
- Neuronal migration and its disorders affecting the CA3 region.Frontiers in cellular neuroscience · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Type I lissencephaly is a central nervous system (CNS) malformation characterized by mental retardation and epilepsy. These clinical features suggest a deficit in inhibitory neurons may, in part, underlie the pathogenesis of this disorder. Mutations in, or deletions of, LIS1 are the most commonly recognized genetic anomaly associated with type I lissencephaly. The pathogenesis of type I lissencephaly is believed to be a defect in radial neuronal migration, a process requiring LIS1. In contrast the inhibitory neurons migrate non-radially from the basal forebrain to the neocortex and hippocampus. Given that Lis1 is expressed in all neurons, we hypothesized that Lis1 also functions in non-radial migrating inhibitory neurons. To test this hypothesis we used a combination of in vivo and in vitro studies with Lis1 mutant mice and found non-radial cell migration is also affected. Our data indicate Lis1 is required for normal non-radial neural migration and that the Lis1 requirement is primarily cell autonomous, although a small cell non-autonomous effect could not be excluded. These data indicate inhibitory neuron migration is slowed but not absent, similar to that found for radial cell migration. We propose that the defect in non-radial cell migration is likely to contribute to the clinical phenotype observed in individuals with a LIS1 mutation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.