Glutamate uptake and potential release via Na + -dependent glutamate transporters is crucial to CNS function and to various forms of injury. Evidence for glutamatemediated damage of oligodendroglia somata and processes in white matter suggests that glutamate regulation in white matter is of particular clinical importance. The expression of glutamate transporters was examined in developing mouse and mature mouse and rat white matter using immuno-histochemistry and immuno-electron microscopy. EAAC1 was the major glutamate transporter detected in oligodendroglia cell membranes in both neonatal and mature optic nerve while GLT1 was the most heavily expressed transporter in the membranes of astrocytes. Both EAAC1 and GLAST were also seen in adult astrocytes but there was little membrane expression of either in the neonate. GLAST, EAAC1 and GLT1 were expressed in neonatal axons with significant amount of GLT1 present in the axolemma, while in mature axons EAAC1 was abundant at the node of Ranvier. Functional glutamate transport was probed in developing mouse optic nerve revealing Na + -dependent, TBOA-blockable uptake of D-aspartate in astrocytes, axons and oligodendrocytes. The data show that in addition to oligodendroglia and astrocytes, axons represent a significant potential sink and source for extracellular glutamate in white matter.

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