ArticleVisual neuroscience
Laminin deficits induce alterations in the development of dopaminergic neurons in the mouse retina.
Article in Visual neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Cellular and Molecular Mechanisms Regulating Retinal Synapse Development.Annual review of vision science · 2024Review
- Laminin N-terminus α31 expression during development is lethal and causes widespread tissue-specific defects in a transgenic mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Laminin β2 Chain Regulates Cell Cycle Dynamics in the Developing Retina.Frontiers in cell and developmental biology · 2021Article
- Eyes shut homolog (EYS) interacts with matriglycan of O-mannosyl glycans whose deficiency results in EYS mislocalization and degeneration of photoreceptors.Scientific reports · 2020Article
- Basement Membrane Changes in Ischemic Stroke.Stroke · 2020Review
- Extracellular Control of Radial Glia Proliferation and Scaffolding During Cortical Development and Pathology.Frontiers in cell and developmental biology · 2020Review
- Laminin β2 Chain Regulates Retinal Progenitor Cell Mitotic Spindle Orientation via Dystroglycan.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Laminin γ3 plays an important role in retinal lamination, photoreceptor organisation and ganglion cell differentiation.Cell death & disease · 2018Article
- Laminin-Dependent Interaction between Astrocytes and Microglia: A Role in Retinal Angiogenesis.The American journal of pathology · 2017Article
- Laminin: loss-of-function studies.Cellular and molecular life sciences : CMLS · 2017Review
- Knockdown of Laminin gamma-3 (Lamc3) impairs motoneuron guidance in the zebrafish embryo.Wellcome open research · 2017Article
- Laminins containing the β2 and γ3 chains regulate astrocyte migration and angiogenesis in the retina.Development (Cambridge, England) · 2013Article
- Recessive LAMC3 mutations cause malformations of occipital cortical development.Nature genetics · 2011Article
- Basement membrane deposition of nidogen 1 but not nidogen 2 requires the nidogen binding module of the laminin gamma1 chain.The Journal of biological chemistry · 2011Article
- Genetic deletion of laminin isoforms β2 and γ3 induces a reduction in Kir4.1 and aquaporin-4 expression and function in the retina.PloS one · 2011Article
- Lack of protein-tyrosine sulfation disrupts photoreceptor outer segment morphogenesis, retinal function and retinal anatomy.The European journal of neuroscience · 2010Article
- Retinal ectopias and mechanically weakened basement membrane in a mouse model of muscle-eye-brain (MEB) disease congenital muscular dystrophy.Molecular vision · 2010Article
- Mutations in Lama1 disrupt retinal vascular development and inner limiting membrane formation.The Journal of biological chemistry · 2010Article
- Defective formation of the inner limiting membrane in laminin beta2- and gamma3-null mice produces retinal dysplasia.Investigative ophthalmology & visual science · 2010Article
- Laminin isoforms containing the gamma3 chain are unable to bind to integrins due to the absence of the glutamic acid residue conserved in the C-terminal regions of the gamma1 and gamma2 chains.The Journal of biological chemistry · 2008Article
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Authors and funding
6 authors.
Funding
Abstract
Genetically modified mice lacking the beta2 laminin chain (beta2null), the gamma3 laminin chain (gamma3 null), or both beta2/gamma3 chains (compound null) were produced. The development of tyrosine hydroxylase (TH) immunoreactive neurons in these mouse lines was studied between birth and postnatal day (P) 20. Compared to wild type mice, no alterations were seen in gamma3 null mice. In beta2 null mice, however, the large, type I TH neurons appeared later in development, were at a lower density and had reduced TH immunoreactivity, although TH process number and size were not altered. In the compound null mouse, the same changes were observed together with reduced TH process outgrowth. Surprisingly, in the smaller, type II TH neurons, TH immunoreactivity was increased in laminin-deficient compared to wild type mice. Other retinal defects we observed were a patchy disruption of the inner limiting retinal basement membrane and a disoriented growth of Müller glial cells. Starburst and AII type amacrine cells were not apparently altered in laminin-deficient relative to wild type mice. We postulate that laminin-dependent developmental signals are conveyed to TH amacrine neurons through intermediate cell types, perhaps the Müller glial cell and/or the retinal ganglion cell.
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