It has been suggested that GABAergic system was involved in ethanol tolerance and addiction. Our previous work indicated both acute and chronic ethanol treatment enhanced the activity of GABA transporters in mouse brain. However, the expression level of GAT1 in CNS does not change, neither does the affinity of GABA transporters. In the present study, we demonstrated that GAT1 distribution on presynaptic membrane was altered after acute and chronic ethanol administration. Furthermore, the phosphorylation levels of GAT1 on three sites including Ser, Tyr and Thr were decreased. These data suggested that ethanol enhanced the function of GATs by means of inducing GAT1 redistribution in the cell and dephosphorylation may play a role in this process.
|Original language||English (US)|
|Number of pages||6|
|Journal||Shi yan sheng wu xue bao|
|State||Published - Aug 2004|
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