Glycine release from Y79 retinoblastoma cells.

Glycine release, induced by a high concentration of potassium chloride (K+), was investigated in cultured human Y79 retinoblastoma cells. The cells were labeled by incubation with [2-3H]glycine prior to K+ depolarization. Depolarization with 55 mM K+ caused an immediate, Ca2+-dependent release of approximately 20% of the cellular radiolabeled glycine content. Chemical analysis of the intracellular free glycine content also showed that approximately 20%, 2.4 nmol/mg protein, was released after K+ depolarization. Glycine release from labeled Y79 cells was not stimulated by incubation with 55 mM choline chloride. Based on measurements with an amino acid analyzer, it is concluded that of the free amino acids contained in the Y79 cell, only glycine is specifically released into the extracellular fluid by K+ depolarization. Although the intracellular content of serine and glutamate decreased, these amino acids were not released from the cells. Further studies with [U-14C]serine suggest that serine is converted into glycine in Y79 cells. Veratridine also caused an immediate release of [2-3H]glycine from the cells, and this was blocked by tetrodotoxin. This suggests that the Y79 cells possess voltage-dependent Na+ channels. These results indicate that K+- and veratridine-stimulated glycine release occurs in Y79 retinoblastoma cells, providing additional evidence that this continuously cultured line may be a useful model for certain human retinal and central nervous system functions.