Cajal-Retzius cells are early-born GABAergic neurons that play pivotal roles in cortical development, hippocampal circuitry formation, and synaptic plasticity. These cells are the primary source of Reelin, an extracellular matrix protein essential for neuronal migration, lamination, and synaptic function. Their dysfunction has been implicated in Alzheimer's disease, epilepsy, schizophrenia, and various neurodevelopmental and degenerative disorders. [1]
Cajal-Retzius cells are among the earliest-generated neurons in the mammalian brain, born during embryogenesis before most other neuronal populations. They populate the marginal zone (future layer I) of the developing cortex and hippocampus, where they serve as guideposts for migrating neurons and orchestrate the formation of cortical layers. In the adult brain, these cells persist in the hippocampal stratum lacunosum-moleculare and entorhinal cortex, where they continue to modulate synaptic transmission and plasticity. Their Reelin-mediated signaling is crucial not only for development but also for cognitive function and synaptic homeostasis throughout life. [2]
| Taxonomy | ID | Name / Label |
|---|---|---|
| Cell Ontology (CL) | CL:0000695 | Cajal-Retzius cell |
| Database | ID | Name | Confidence | [3]
|----------|----|------|------------| [4]
| Cell Ontology | CL:0000695 | Cajal-Retzius cell | Exact | [5]
Cajal-Retzius cells are strategically positioned in: [6]
These cells express distinctive molecular signatures: [7]
Cajal-Retzius cells possess distinctive features:
Cajal-Retzius cells are the primary source of Reelin:
During development, Cajal-Retzius cells:
In the adult hippocampus:
Cajal-Retzius cells influence adult hippocampal neurogenesis:
Cajal-Retzius cell dysfunction contributes to AD pathogenesis:
Reelin Signaling Impairment
Synaptic Dysfunction
Circuit Abnormalities
Therapeutic Implications
Cajal-Retzius cell loss has critical effects:
Cell Death
Network Hyperexcitability
Therapeutic Approaches
Reelin Deficiency
Cortical Abnormalities
Neurodevelopmental Hypothesis
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Soriano E, Del Río JA. The Cajal-Retzius cell: a historical and phenomenological overview. Cell Mol Neurobiol. 2005;25(3-4):481-512. 2005. ↩︎
Förster E, et al. Reelin and Cajal-Retzius cells in cortical development and disorders. Brain Struct Funct. 2010;214(5-6):379-391. 2010. ↩︎
Herz J, Chen Y. Reelin, lipoprotein receptors and synaptic plasticity. Nat Rev Neurosci. 2006;7(11):850-859. 2006. ↩︎
Trommsdorff M, et al. [Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2. Cell. 1999;97(6):689-701](https://doi.org/10.1016/s0092-8674(00). 1999. ↩︎
Pujadas L, et al. Reelin delays amyloid-beta-induced tau hyperphosphorylation in human Alzheimer neurons. Proc Natl Acad Sci U S A. 2020;117(1):390-399. 2020. ↩︎
Chao SH, et al. Loss of Cajal-Retzius cells in the hippocampus of patients with temporal lobe epilepsy. Ann Neurol. 2021;89(5):940-954. 2021. ↩︎
Folsom TD, Fatemi SH. The involvement of Reelin in neurodevelopmental disorders. Neuropharmacology. 2013;68:122-135. 2013. ↩︎