PMID: 8947947Nov 1, 1996Paper

Attenuation of trimethyltin-evoked glutamate (GLU) efflux from rat cortical and hippocampal slices

Neurotoxicology and Teratology
T A PattersonR Dawson

Abstract

Trimethyltin (TMT) is a toxic alkyltin that produces neuronal necrosis in the CNS. TMT stimulates the efflux of the excitatory amino acid glutamate (GLU) from rat cortical slices. This release is concentration dependent, partially calcium dependent, but not inhibited by calcium channel blockers or a NMDA antagonist. In the present study the compounds furosemide, bumetanide, 4,4'-diisothiocy-anatostilbene-2,2'-disulfonic acid (DIDS), and DL-threo-beta-hydroxyaspartic acid (HAA) were tested for their ability to attenuate TMT-stimulated GLU efflux from rat cortical and hippocampal slices. Furosemide (1 mM) reduced the TMT-induced GLU efflux in cortical slices and hippocampal slices, but bumetanide (0.1 mM) had no effect on TMT-induced GLU efflux. DIDS (1 mM) demonstrated a trend toward decreasing GLU efflux from TMT stimulation in both the cortex and hippocampus, but this reduction was not significant. However, DIDS was able to prevent the decrease in intracellular GLU content produced by TMT in both the cortical and hippocampal slices. HAA (1 mM) increased the net GLU efflux in both cortical slices and hippocampal slices, and produced a significant depletion of the glutamate content of the slices. Taurine efflux was stimulated by...Continue Reading

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Citations

Feb 1, 2003·Archives of Biochemistry and Biophysics·Songmin Cai, Donald W Horne

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