NEURONAL GLIAL EXCHANGE OF TAURINE DURING HYPOOSMOTIC STRESS - A COMBINED IMMUNOCYTOCHEMICAL AND BIOCHEMICAL-ANALYSIS IN RAT CEREBELLAR CORTEX

Rat cerebellar Purkinje cells show a high level of taurine-like immuno reactivity. Light-microscopic immunocytochemisty indicated that the le vel of taurine in these cells was substantially decreased in animals t hat had survived for 4 h after an intraperitoneal injection of distill ed water. This treatment resulted in a 15-20% reduction in plasma osmo lality. The changes in the Purkinje cells were accompanied by an incre ased immunolabeling of neighboring glial cells (Golgi epithelial cells ). The changes in both cell types were reversed in animals whose plasm a osmolality had been normalized by injections of hypertonic saline 4 h after the water loading. Adjacent sections incubated with a GABA ant iserum did not exhibit any overt changes in response to the hypo-osmot ic stress.Quantitative electron-microscopic analysis of ultrathin sect ions subjected to postembedding immunogold cytochemistry indicated tha t the Purkinje cells had lost 50-60% of their taurine contents after w ater loading and that the loss affected all intracellular compartments , including mitochondria and cytoplasmic matrix. The loss of taurine i mmunoreactivity from Purkinje cells was accompanied by an estimated 70 -80% increase in the contents of immunoreactive taurine in adjacent gl ial cells. Biochemical recordings of tissue amino acids in a parallel series of animals revealed a 12% reduction in cerebellar taurine conte nts 4 h after water loading (value corrected for changes in specific g ravity). This reduction had progressed to 32% after 8 h and was only p artly prevented by normalization of plasma osmolality. The tissue leve ls of GABA and several other amino acids showed a decrease similar to that of taurine, while glutamine displayed a considerable increase aft er water loading. Our findings indicate that acute reductions in plasm a osmolality cause a flux of taurine from Purkinje cells to glia, and that this flux is reversed upon normalization of plasma osmolality. Th ese changes are superimposed on a decrease in the biochemically record ed tissue level of taurine. Unlike the cellular redistribution, this d ecrease was not reversible within the time frame of the present study, and it was not specific for taurine. Cellular redistribution of tauri ne may represent a rapid adjustment to osmotic perturbations in vivo. In addition, it may reflect a higher priority for neuronal compared wi th glial volume regulation.