Glutamate Release by Reversed Glutamate Uptake Is Inhibited by Arachidonic Acid

Abstract

Glutamate uptake into neurones and glia helps to terminate the synaptic action of neurotransmitter glutamate and to keep the extracellular glutamate concentration below levels which are neurotoxic. Recently we have shown [1] that glutamate uptake into glial cells can be monitored as a membrane current using whole-cell patch clamping. This technique depends on the fact that the glutamate uptake carrier transports a net positive charge into the cell on each carrier cycle: the carrier is thought to transport three sodium ions (or possibly two Na⁺ and one proton [2]) into the cell with each glutamate anion, and to transport one potassium ion out of the cell [3]. Using whole-cell patch clamping to study glutamate uptake allows uptake to be studied under voltage-clamp conditions (which is important because membrane potential is a crucial determinant of the rate of uptake [1]) and allows the composition of the cell contents to be controlled via the patch pipette (a facility which is employed in the experiments reported below).

This study was supported by the Wellcome Trust, the MRC, the SERC and the Wolfson Foundation.