TAURINE DEFICIENCY IN DISSOCIATED MOUSE CEREBELLAR CULTURES AFFECTS NEURONAL MIGRATION

The role of taurine in the process of neuronal migration was studied i n a microwell cell culture system, Immunocytochemical analysis of the cellular composition of this culture system revealed the presence of t he astrocytic marker GFAP in some structures such as the aggregates of neuronal bodies and in those cables used for migration, resembling wh at is described in vivo. The neuronal marker gamma-enolase stained pra ctically all structures, including the aggregates and all cables. The intracellular taurine concentration was reduced by 60% in mouse cerebe llar granule cells treated with a blocker of taurine transport, guanid inoethane sulfonate (GES). Under these conditions cell migration was m arkedly reduced to approximately 50% of that in untrated cultures. Bot h, taurine depletion and impairment of cell migration induced by GES w ere prevented by adding taurine to the culture medium. Taurine deficie ncy similarly affected different morphological parameters such as the number of cables suitable for neuronal migration as well as the number of migrating neurons. The number of aggregates of neuronal bodies was significantly increased, by about 30%, as a consequence of the reduce d migration. Taurine alone did not exert any effect on the parameters evaluated. GES treatment of granule cells did not affect mitochondrial metabolism or K+-stimulated Ca2+-dependent [H-3]-D-aspartate release. This suggests that the described effects of taurine deficiency were n ot due to an alteration of neuronal viability and that the action of G ES was not simply due to unspecific and deleterious effects. These res ults are in agreement with those obtained in in vivo studies. This app roach represents a useful model to investigate the role played by taur ine in the process of neuronal migration.