engleski

Role of glycolipids in brain development and regeneration

Introduction: Appearance of glycolipids in developing brain follows the strict order. Inactivation of Galgt1 gene prevents synthesis of complex gangliosides – markers of mature neurons and reduces regular developmental sequence of glycolipid synthesis to only GD3. These knockout mice develop without neurological abnormalities up to the age of six months after which they have significant demyelization and epileptic seizures. Galgt1 knockout have just one (GD3) out of possible three (GD3, GD1a and GT1b) glycolipid ligands for MAG – an oligodendrocyte receptor having a role in the maintenance of compact myelin. To further investigate the role of glycolipids in the stability of myelin we compared wild types with three different knockouts: Galgt1, Siat8 and St3gal2 differently expressing possible ligands. Materials and Methods: Serial sections of wild type and knockout brains (Galgt1, Siat8 and St3gal2) were immnunostained for complex gangliosides and markers of myelin maturation. Some myelinated fiber tracts have been subjected to further electron microscopy analysis. Results: Wild type animals express GD3, GD1a and GT1b on neuronal bodies and fiber tracts up to PND10 – the onset of myelination. After beginning of myelination GD1a is colocalized with MAG only in the middle of corpus callosum in wild types and in the most of fiber tracts in the half of studied Siat8 animals. Conclusion: In adult animals GD3 is probably not physiological ligand for MAG. After PND10 possible ligands are GD1a and GT1b, but only on some fiber tracts. Siat8 animals expressing GD1a in the most of fiber tracts also express markers of immature myelin.

glycolipids; development; regeneration

Časopis je indeksiran u Neuroscience Citation indeksu i EMBASE/Excerpta Medica.