ArticleNeuroscience2011
Disturbances in the positioning, proliferation and apoptosis of neural progenitors contribute to subcortical band heterotopia formation.
Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 39 citations in OpenAlex.
- Impaired neurogenesis and neural progenitor fate choice in a human stem cell model of SETBP1 disorder.Molecular autism · 2023Article
- A deletion in Eml1 leads to bilateral subcortical heterotopia in the tish rat.Neurobiology of disease · 2020Article
- Pathological characteristics of Ccdc85c knockout rats: a rat model of genetic hydrocephalus.Experimental animals · 2020Article
- The Thymus/Neocortex Hypothesis of the Brain: A Cell Basis for Recognition and Instruction of Self.Frontiers in cellular neuroscience · 2017Article
- Neuronal migration disorders: Focus on the cytoskeleton and epilepsy.Neurobiology of disease · 2016Review
- Causes and consequences of gray matter heterotopia.CNS neuroscience & therapeutics · 2015Review
- Mutations in Eml1 lead to ectopic progenitors and neuronal heterotopia in mouse and human.Nature neuroscience · 2014Article
- TAG-1-assisted progenitor elongation streamlines nuclear migration to optimize subapical crowding.Nature neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cortical malformations are commonly associated with intractable epilepsy and other developmental disorders. Our studies utilize the tish rat, a spontaneously occurring genetic model of subcortical band heterotopia (SBH) associated with epilepsy, to evaluate the developmental events underlying SBH formation in the neocortex. Our results demonstrate that Pax6(+) and Tbr2(+) progenitors are mislocalized in tish(+/-) and tish(-/-)- neocortex throughout neurogenesis. In addition, mislocalized tish(-/-) progenitors possess a longer cell cycle than wild type or normally-positioned tish(-/-) progenitors, owing to a lengthened G(2)+M+G(1) time. This mislocalization is not associated with adherens junction breakdown or loss of radial glial polarity in the ventricular zone (VZ), as assessed by immunohistochemistry against phalloidin (to identify F-actin), aPKC-λ and Par3. However, vimentin immunohistochemistry indicates that the radial glial scaffold is disrupted in the region of the tish(-/-) heterotopia. Moreover, lineage tracing experiments using in utero electroporation in tish(-/-) neocortex demonstrate that mislocalized progenitors do not retain contact with the ventricular surface and that ventricular/subventricular zone (SVZ) progenitors produce neurons that migrate into both the heterotopia and cortical plate (CP). Taken together, these findings define a series of developmental errors contributing to SBH formation that differs fundamentally from a primary error in neuronal migration.
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