[12] Immunohistochemical studies (detecting antigens by exploiting the principle of antibodies binding specifically to antigens in biological tissues) showed that CR cells expressed GABA-A and GABA-B receptors,[13] ionotropic and metabotropic glutamate receptors,[13] vesicular glutamate transporters,[14] and a number of different calcium-binding proteins, such as calbindin, calretinin and parvalbumin.

[17] Using chloride-containing patch-clamp electrodes in 2006, spontaneous postsynaptic currents (PSCs) were recorded in about 30% of the CR cells in P0-P2 rat cerebral cortex.

Therefore, CR cells control two processes: detachment from radial glia and somal translocation in the formation of cortical layers.

In addition, the reeler type also manifests a poor organization of the Purkinje cell plate(PP) and the inferior olivary complex(IOC).

It exhibits some behavioral abnormalities, such as ataxia, tremor and hypotonia, which were discovered to be related to problems in neuronal migration and consequently, cytoarchitecture in the cerebellum, hippocampus and cerebral cortex.

[15][19][20] It was found later that the mutation causing these disorders was located in the RELN gene which codes for reelin, a glycoprotein secreted by Cajal–Retzius cells in the developing brain.

[15] When the mutation occurs, reelin expression is reduced and this signal isn't as strong, therefore, migration of the first neurons in the brain is not done correctly.

[21] In 1891 Santiago Ramón y Cajal described slender horizontal bipolar cells he had found in an histological preparation of the developing marginal zone of lagomorphs.

[38][40][41][42] Various studies then proved the Cajal–Retzius cells as being responsible for the production of reelin,[42][43][44] In 1999, Meyer loosely defined the Cajal–Retzius cells as the family of Reln-immunoreactive neurons in the marginal zone of the hippocampus,[45] as so to settle a difference between the pioneer neurons, Reln-negative preplate derivatives that settle in the same area and project to the subcortical area that he had already described in 1998.

[45] In 2005, the discovery of heterogeneous transcription factors and new sites of origin suggested that there were distinct subpopulations of Cajal–Retzius cells in different territories of the developing cortex.