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As a result, glutamate uptake produces net inward current. Expression in oocytes has enabled detailed study of their properties and provided evidence that glutamate transport is driven by the coupled cotransport of three Na + and one H + and the countertransport of one K + ( Zerangue and Kavanaugh, 1996 Levy et al., 1998). To date, five glutamate transporter subtypes have been identified, called EAAT (excitatory amino acid transporter) 1–5. Glutamate reuptake is mediated by high-affinity transporters that are present in neuronal and glial membranes (for review, see Danbolt, 2001). Glutamate transporter currents with rapid kinetics are therefore identified and characterized in bipolar cell terminals, providing a valuable system for investigating the function and modulation of presynaptic glutamate transporters.

In contrast, neither exocytosis nor exogenous glutamate evoked a transporter current in the calyx of Held.

The large single-channel conductance, derived from noise analysis, and previous immunolocalization studies suggest that synaptically released glutamate activates EAAT5-type transporters in bipolar cell terminals. A TBOA-sensitive anion current was also evoked by application of exogenous glutamate to bipolar cell terminals. It was inhibited by the nontransportable glutamate transporter antagonist sc- threo-β-benzyloxyaspartate (TBOA) but was insensitive to the GLT1/EAAT2 subtype-selective antagonist dihydrokainate and was affected by extracellular pH buffering. The current peaked 2.8 msec after the start of the depolarization and decayed with a mean time constant of 8.5 msec. In isolated bipolar cell terminals, exocytosis was associated with an anion (NO 3 - or Cl -) current. Exocytosis was evoked by brief depolarizations and measured as an increase in membrane capacitance. Here, we have recorded from two giant nerve terminals: bipolar cell synaptic terminals in goldfish retina and the calyx of Held in rat auditory brainstem. However, less is known about presynaptic transporter currents because the small size of synaptic boutons precludes direct recordings. The reuptake process generates membrane currents, which can be activated by synaptically released glutamate in glial cells and some postsynaptic neurons. Glutamate uptake by high-affinity transporters is responsible for limiting the activation of postsynaptic receptors and maintaining low levels of ambient glutamate.

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