Taurine Deficiency and Neuronal Migration

Abstract

Cerebellar granule neurons migrate from the external layer to the internal granule layer along the processes of Bergmann fibers14, 15. It is known from a number of studies that this is a finely modulated process of cell-cell interaction controlled by a variety of external conditions. This event involves cell surface molecules on both neurons and glia, including extracellular matrix molecules, neural cell adhesion molecules (NCAM), and some members of the integrin and cadherin families1, 3, 6, 13, 19, 20. Numerous observations in vitro and in vivo document the involvement of taurine in the process of neuronal migration. This process may be disturbed or even prevented by reducing the cerebellar taurine content which normally is high during early development17, 18. This relationship between taurine and granule cell migration has been particularly well studied in the cat17, 18, a species especially vulnerable to taurine deficiency by removal of taurine from the diet4. Taurine depletion, however, is a slow process, requiring several months to be completed. We have previously reported a simple and rapid model of taurine deficiency in an in vitro system by preventing cellular taurine uptake by guanidinoethane sulfonate (GES)5, 10. The present study has utilized an in vitro system to investigate the role of taurine for cell migration, aggregate formation, and the expression of NCAM in cerebellar cells employing GES to render the cultures taurine deficient.