The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Time of origin of corresponding cell classes in the cerebral cortex of normal and reeler mutant mice: An autoradiographic analysis
Abstract
Reeler, a recessive mutation in mice, causes cytoarchitectonic abnormalities of the cerebral and cerebellar cortices. Although the relative positions of classes of cells in the cerebral cortex are markedly abnormal, the time of origin of cells in each class appears to be normal by autoradiographic criteria. In the retrohippocampal cortical structures and in the adjacent neocortex, the earliest generated cell class, the polymorphic, arises at the same embryonic time in normal and reeler littermates. Whereas these cells come to form the deepest stratum of the normal cortex, they lie in an immediately subpial position in the mutant, there being no cell‐sparse external plexiform (molecular) layer. A population of larger cells is generated next; these normally come to lie in more superficial layers but instead lie deep to the polymorphic cells in the mutant. Granule cells of the neocortex arise last, simultaneously in normal and reeler; they form the most superficial neocortical cell stratum in the normal, but lie at a more restricted level within the large cell zone in the mutant. These data indicate that the cytoarchitectonic anomaly in reeler is independent of the spatiotemporal program of cell generation. It appears likely that the reeler genetic locus governs embryonic events, as yet undefined, that direct the postmitotic migrating young neuron to class‐specific levels within the cortex.
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“The reeler is an autosomal recessive mouse mutant, in which neurons are generated normally but are abnormally placed, resulting in disorganization of cortical laminar layers in the CNS (7–12).”
From Reelin molecules assemble together to form a large protein complex, which is inhibited by the function-blocking CR-50 antibody (2000) · cites this paper as [11]
In the citing paper
“in the reeler mouse model, in which expression of reelin or associated proteins is disrupted, the lamination of PCs in cortex is inverted and the s.p. of the hippocampus is split in region CA1”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [180]
Citations
Cites
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Self-citationATLAS OF THE MOUSE BRAIN AND SPINAL CORD
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Sidman, R. L. (1970) · Springer eBooks · doi:10.1007/978-3-642-85986-1_12 · Cited by 312
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- Kölliker A., 1896, Handbuch der Gewebelehre des Menschen
- Sidman R. L., 1968, Expanding Concepts in Mental Retardation, 40
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Radial migration in the developing cerebral cortex
Noctor, S. C., Cunningham, C. L., & Kriegstein, A. R. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-814407-7.00015-8 · Cited by 2
The Normal and Abnormal Development of the Mammalian Visual System
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Nowakowski, R. S. (2023) · Developmental Neuroscience · doi:10.1159/000531759
Thyroid Hormone-Regulated Genes in the Brain
Bernal, J. (2024) · BENTHAM SCIENCE PUBLISHERS eBooks · doi:10.2174/9789815274226124010014
NUBP2 deficiency disrupts the centrosome-check point in the brain and causes primary microcephalyPreprint
Rushforth, R., Shamseldin, H. E., Costantino, N., Michaels, J.-R., Sawyer, S. L., Osmond, M., Kurdi, W., Abdulwahab, F., DiStasio, A., Boycott, K. M., et al. (2025) · medRxiv · doi:10.1101/2025.01.16.25320041
Early Postnatally Induced Conditional Reelin Deficiency Causes Malformations of Hippocampal Neurons
Lódi, M., Ahrari, A., Meseke, M., Corvace, F., Kümmel, M.-L., Trampe, A.-K., Hamad, M. I. K., & Förster, E. (2025) · Biomolecules · doi:10.3390/biom15121662
Betizeau, M. (2013) · theses.fr (ABES) · doi:10.70675/96b2fd4ez61cfz4afeza473z7811a8b1fda6
Génétique et physiopathologie du syndrome de Lowe, analyse des aspects neurologiques
Héritier, A. (2019) · theses.fr (ABES) · doi:10.70675/de6a261fz5927z43bdza3cez77bae3ad1666
Development and specification of cortical areas in the non human primate
Pace, C. (2020) · theses.fr (ABES) · doi:10.70675/b7094400z9034z4ec5zb776zde051009bafa
Salin (1998) · doi:10.1002/(sici)1096-9861(19980720)397:1
Metadata
- Authors
- Caviness, V. S., & Sidman, R. L.
- Affiliations
- Harvard University (US)
- ORCID
- Sidman, R. L.
- Venue
- Journal of Comparative Neurology
- Publisher
- Wiley
- Published
- 1973-03-15
- Volume
- 148
- Issue
- 2
- Pages
- 141-151
- ISSN
- 0021-9967 (ISSN-L)
- 1096-9861
- OpenAlex
- W1994406909
- Cited by
- 413
- References
- 17
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 5 · 2018: 3 · 2017: 10 · 2016: 6 · 2015: 10 · 2014: 13 · 2013: 15 · 2012: 10
- FWCI
- 3.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Comparative Neurology (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Fetal and Pediatric Neurological Disorders
- Keywords
- cerebral cortex, cell migration, cytoarchitecture, granule cells, cortical layers, neocortex, cerebellum, embryonic development
- MeSH terms
- Animals, Autoradiography, Cell Differentiation, Cerebral Cortex, Hippocampus, Movement Disorders, Neurons, Thymidine, Mice
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