Cajal–Retzius cell
From NeuronBankWiki
Cajal–Retzius cell is a neuron of the human embryonic marginal zone of the Brain that produces Reelin-producing neurons of the human embryonic which show, as a salient feature, radial ascending processes that connect the Pia Mater, and a horizontal axon plexus located in the deep marginal zone. These cells were first described by Gustaf Retzius (Retzius, 1893, 1894).
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Basic information
- Names and Aliases: Retzius Cells; Cajal-Retzius Cell; Neocortex Cajal-Retzius cell
- Species: All Amniotes
- Protein Involved: Reelin
- Neuronal Type: Sensory Neuron, Motor Neuron, Interneuron
Anatomy
Large star-shaped cell found in the more superficial marginal zone of the preplate; this is found just beneath the pial surface. Cajal–Retzius cells possess very long horizontal axons that form asymmetric synaptic contacts with dendritic shafts or spines of neocortical pyramidal cells. Although their exact origin remains a subject of controversy, the caudomedial wall of the telencephalic vesicle has been proposed as the primary source.
History
Cajal-Retzius Cells were initially described by Santiago Ramón y Cajal in 1891. They were decribed as slender horizontal bipolar cells in the developing marginal zone of lagomorphs. These cells were considered by Retzius as homologues to the cells he found in humans and in other mammals (Retzius, 1893, 1894). Similar cells are also present in the rodent marginal zone.
Role in the cortex
CR cells establish early neuronal circuitry in the developing brain (Aguiló et al., 1999), and express a number of genes known to be important in human cerebral development:
- LIS1 (Clark et al., 1997), which is mutated in lissencephaly;
- EMX2 (Mallamaci et al., 1998);
- Fukutin;[1]
- RELN (Meyer and Goffinet, 1998). The gene RELN encodes the protein reelin, which is secreted extracellularly by layer I neurones through a constitutive, nonvesicular mechanism (Lacor et al., 2000). This extracellular matrix protein, which is also secreted by Cajal–Retzius neurons, serves as a signal to dissociate for migrating neurons, which travel in clusters, and controls the formation of cortical layers. Lack of reelin, as in the reeler mouse mutant, disturbance of the reelin signaling pathway or ablation of Cajal–Retzius cells causes disorders in cortical lamination.
- HAR1F
- P73 protein, a p53-family member involved in the processes of cell survival and apoptosis.[2]
Chameau et al. (2009) report that Cajal–Retzius cells postnatally receive a major excitatory synaptic input via 5-HT3 receptors,[3] and that abolishing this interaction deregulates cortical development, leading to an overgrowth of apical dendrites of layer 2\3 pyramidal cells.
References
- Chameau P, Inta D, Vitalis T, Monyer H, Wadmann W, van Hooft J. The N-terminal region of reelin regulates postnatal dendritic maturation of cortical pyramidal neurons. Proceedings of the National Academy of Sciences of the United States of America [serial online]. April 28, 2009;106(17):7227-7232. Available from: Academic Search Complete, Ipswich, MA. Accessed August 29, 2009.
- Chameau P., Inta D., Vitalis T., Monyer H., Wadman W., van Hooft J.. The N-terminal region of reelin regulates postnatal dendritic maturation of cortical pyramidal neurons. Proceedings of the National Academy of Sciences of the United States of America [serial online]. 2009;106:7227. Available from: Research Library. Accessed August 29, 2009, Document ID: 1692455151.
- Huang Z. Molecular regulation of neuronal migration during neocortical development. MCN: Molecular & Cellular Neuroscience [serial online]. August 2009;42(1):11-22. Available from: Academic Search Complete, Ipswich, MA. Accessed August 29, 2009.
- Medina L, Abellán A. Development and evolution of the pallium. Seminars in Cell & Developmental Biology [serial online]. August 2009;20(6):698-711. Available from: Academic Search Complete, Ipswich, MA. Accessed August 29, 2009.
- Sanes, Dan H., Thomas A. Reh, and Harris, William A. Development of the Nervous System, Second Edition. New York: Academic P, 2005.
