Glial transporters for glutamate, glycine, and GABA: II. GABA transporters

The termination of chemical neurotransmission in the central nervous system (CNS) involves the rapid removal of neurotransmitter from synapses. This i s fulfilled by specific transport systems in neurons and glia, including th ose for gamma -aminobutyric acid (GABA), the main inhibitory neurotransmitt er in the brain. Glial cells express the cloned Na+/Cl--dependent, high-aff inity GABA transporters (GATs) GAT1, GAT2, and GAT3, as well as the low-aff inity transporter BGT1. in situ hybridization and immunocytochemistry have revealed that each transporter shows distinct regional distribution in the brain and the retina. The neuronal vs. glial localization of the different transporters is not clear-cut, and variations according to species, neighbo ring excitatory synapses, and developmental stage have been reported. The l ocalization, stoichiometry, and regulation of glial GATs are outlined, and the participation of these structures in development, osmoregulation, and n europrotection are discussed. A decrease in GABAergic neurotransmission has been implicated in the pathophysiology of several CNS disorders, particula rly in epilepsy. Since drugs which selectively inhibit glial but not neuron al GABA uptake exert anticonvulsant activity, clearly the establishment of the molecular mechanisms controlling GATs in glial cells will be an aid in the chemical treatment of several CNS-related diseases. J. Neurosci. Res. 6 3: 461-468, 2001, (C) 2001 Wiley-Liss, Inc.