HISTOLOGICAL, ULTRASTRUCTURAL AND IMMUNOCITOCHEMICAL CHARACTERIZATION OF THE POST-NATAL DEVELOPMENT IN THE REELER MOUSE

Reelin, a protein necessary for the correct neuronal migration in several brain areas with laminar architecture, is missing in the reeler mouse (reeler-/-). Therefore, the mutant mouse is an appropriate model to study the mechanisms involved in the neuronal migration and cortical lamination and it is considered a good model for neurological disorders such as autism. The aim of this study was to characterize the development of the cerebellum of the reeler mouse from birth to adulthood. The cerebellum of these animals is reduced in size (both in vermis and hemispheres), folia are completely missing and the lamination of the cortex is incomplete. In particular, the Purkinje neurons fail to migrate and to form a well-defined layer in the cortex and can be detected deeply in the white matter, intermingled with the deep cerebellar nuclei neurons and with some ectopic glial cells. The proliferation/death rate typical of the post-natal development of the wild type mouse is also alterated: the immunocitochemical analysis by means of neuronal markers (Pax-6, NeuN, Smi-32, calbindin) demonstrates that the more affected cells are the Purkinje neurons. Ultrastructural analysis indicates that the synaptic connections are altered in terms of morphology and position. Honda et al., Neurochem.Res. 21 2011 ; Myiata et al., Neural Dev. 1 2010; Badea et al. Neuroimage 15 2007