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γ
Fig. 11.1. Glutamate and
-aminobutyric acid ( GABA ) transporters at synapses. The exci-
tatory neurotransmitter glutamate and the inhibitory neurotransmitter GABA are stored
in synaptic vesicles at presynaptic terminals and released into the synaptic cleft to act
on postsynatptic receptors. High-affinity transporters play an important role in removing
glutamate and GABA released from the synaptic cleft and maintaining the external glu-
tamate and GABA concentrations below neurotoxic levels ( EAAC1 ,sodiumdicarboxylate
symporter superfamily) for glutamate, GAT2 and GAT3 (neurotransmitter superfamily) for
GABA). Glutamate taken up in astroglial cells by GLT and GLAST (sodium dicarboxylate
symporter superfamily) is degraded to glutamine by the glutamine synthetase ( GS ). Glu-
tamine, which can serve as a precursor of glutamate synthesis in the nerve terminal, is
exported from the glial by SN1 (amino acid, AA , transporter superfamily 1, AT F 1 ). In the
neuron glutamine [taken up by GlnT1 , ASC1 and ASC2 (sodium dicarboxylate symporter
superfamily)] is converted to glutamate by a phosphate-activated glutaminase ( PAG ). Neu-
rotransmitters are transported into synaptic vesicles by BNP1 and VGluT1 (major facilitator
superfamily) for glutamate, and VGAT (ATF1) for GABA. Until now it is not clear whether
the presynaptic terminal possess a specialized glutamate transporter. (Reprinted from Wipf
et al. 2002, with permission from Elsevier)
example, EAAT5 (system X AG )isreportedtobeexpressedprimarilyinthe
retina (Arriza et al. 1997), suggesting that the EAAT5 protein is involved
in visual processes (Kanai and Hediger 2004). No SLC1 homologs were
reported in plants.
 
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