N. V. Krisanova, R. V. Sivko, O. A. Krupko, T. A. Borisova
Role of membrane cholesterol in direct and reversed function of Na+-dependent glutamate transporters and exocytosis was investigated. The depletion of membrane cholesterol by methyl-?-cyclodextrin (Me?CD) resulted in a dose-dependent significant reduction of the L-[14C]glutamate uptake by synaptosomes. Treatment of synaptosomes with 15?mM Me?CD caused a decrease in the velocity of L-[14C]glutamate uptake by 49?±?4% (Р???0.05). The depolarization stimulated Ca2+ dependent glutamate release that occurred via reverse functioning of glutamate transporters decreased insignificantly for 1 min from 8.0?±?0.4% to 6.7?±?0.4% of total accumulated synaptosomal label after Me?CD treatment. The depletion of membrane cholesterol resulted in a reduction of the depolarization evoked exocytotic release from 8.0?±?1.0% to 4.2 ± 1.0% of total synaptosomal label. Thus, cholesterol depletion was found to decrease significantly the Na+-dependent uptake and exocytotic release of glutamate.
Key words: cholesterol, methyl-?-cyclodextrin, lipid rufts, glutamate transporters, exocytosis, nerve terminals. The original article in Russian is available for download in PDF format.
The original article in Russian is available for download in PDF format.
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