Cajal-Retzius cell



The term Cajal–Retzius cell is applied to reelin-producing neurons of the human embryonic marginal zone which display, as a salient feature, radial ascending processes that contact the pial surface, and a horizontal axon plexus located in the deep marginal zone. These cells were first described by Retzius (Retzius, 1893, 1894). 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.

Cajal–Retzius cells are found in the marginal zone in all amniotes, which indicates their evolutionary homology. However, mammalian Cajal–Retzius cells produce substantially higher amounts of reelin, pointing to the spatiotemporal control of reelin expression as a key feature of cortical evolution.

History
Cajal described in 1891 slender horizontal bipolar cells in the developing marginal zone of lagomorphs.(See the Cajal's original drawing of the cells) 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;
 * 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.