Early Neocortical Regionalization in the Absence of Thalamic Innervation
Abstract
There is a long-standing controversy regarding the mechanisms that generate the functional subdivisions of the cerebral neocortex. One model proposes that thalamic axonal input specifies these subdivisions; the competing model postulates that patterning mechanisms intrinsic to the dorsal telencephalon generate neocortical regions. Gbx-2 mutant mice, whose thalamic differentiation is disrupted, were investigated. Despite the lack of cortical innervation by thalamic axons, neocortical region–specific gene expression ( Cadherin-6 , EphA-7 , Id-2 , and RZR-beta ) developed normally. This provides evidence that patterning mechanisms intrinsic to the neocortex specify the basic organization of its functional subdivisions.
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Differential gene expression and gradients of signaling molecules across the embryonic brain generate prospective subdivisions of the neocortex.
“More specifically, it is well documented that differential gene expression and the gradients of signaling molecules across the embryonic brain generate prospective subdivisions of the neocortex [24–29].”
From Development of prefrontal cortex (2022) · cites this paper as [28]
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“Gbx2 is essential for repressing Irx genes in postmitotic cells in the thalamus We and others have demonstrated that Gbx2 ablation results in profound defects in the histogenesis of the thalamus and axonal outgrowth and guidance to the neocortex (Miyashita-Lin et al., 1999; Hevner et al., 2002; Chen et al., 2009; Chat…”
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- Authors
- Miyashita-Lin, E. M., Hevner, R., Wassarman, K. M., Martinez, S., & Rubenstein, J. L. R.
- Affiliations
- University of California, San Francisco (US)
- Department of Morphological Sciences, Faculty of Medicine, University of Murcia, Institute of Neurosciences, University Miguel Hernandez, Alicante, Spain.
- Corresponding author
- Miyashita-Lin, Emily M.
- Hevner, Robert
- Wassarman, Karen Montzka
- Rubenstein, John L. R.
- Venue
- Science
- Published
- 1999-08-06
- Volume
- 285
- Issue
- 5429
- Pages
- 906-909
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2071596650
- Cited by
- 349
- References
- 31
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 6 · 2021: 6 · 2020: 5 · 2019: 28 · 2018: 4 · 2017: 7 · 2016: 3 · 2015: 9 · 2014: 7 · 2013: 13 · 2012: 17
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- National Institutes of Health (2r01mh051561-04a1)
- National Institute of Mental Health (R01 MH4942801, R01MH049428, R01MH51561-01A1)
- National Institute of Neurological Disorders and Stroke (R01NS034661, NS34661-01A1)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Keywords
- thalamocortical connections, cortical patterning, dorsal telencephalon, Id2, CDH6
- MeSH terms
- Animals, Axons, Carbocyanines, DNA-Binding Proteins, Immunohistochemistry, Mutation, Nerve Fibers, Proteins, Receptors, Cell Surface, Steroid 17-alpha-Hydroxylase, Telencephalon, Thalamus, Transcription Factors, Cadherins, Gene Expression, In Situ Hybridization, Receptors, Cytoplasmic and Nuclear, Homeodomain Proteins, Neocortex, Receptors, Melatonin, Mice, Inhibitor of Differentiation Proteins, Lymphoid Enhancer-Binding Factor 1, S100 Calcium Binding Protein G, Calbindin 2
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