ISSN:
1432-2013
Keywords:
Apoptosis Cell volume Cerebellar granule neurons Osmolyte efflux Osmoregulation Sodium Taurine
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract. Cell shrinkage is a distinctive feature of apoptotic death, but the mechanisms leading to cell volume loss are unclear at present. Activation of pathways extruding intracellular osmolytes such as K+, Cl– and organic molecules may be part of these mechanisms. This was examined in the present work measuring the release of taurine, γ-amino-butyric acid (GABA) and glutamate in cerebellar granule neurons cultured in conditions resulting in apoptotic death after 4–7 days in vitro (DIV). The basal release of [3H]taurine from cells started to increase (38%) after 3 DIV and reached a maximal enhancement (250%) at 5 DIV. The increase in taurine efflux closely followed the occurrence of apoptotic death markers such as caspase induction and chromatin condensation. The efflux of glutamate (traced as d-aspartate) and [3H]GABA also increased but notably less than that of taurine (90% and 75%, respectively) at 5 DIV. Taurine release associated with apoptosis was unaffected by 4,4'-diisothiocyanatostilbene 2,2'-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), blockers of the diffusive pathway activated during cell volume regulation in hyposmotic conditions. Taurine efflux was increased in Cl–-free (replaced by gluconate) and decreased in Na+-free media. Blockers of the energy-dependent glutamate and taurine carriers, dihydrokainate and guanidinoethane sulfonate, respectively, did not affect the release associated with apoptosis. These results implicate taurine in the mechanism of cell shrinkage during apoptosis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004249900168
Permalink
