GABA transporter type 2

Brain Deletion of the GAT2 gene in mice does not appear to have any dramatic effects on brain function in a normal situation. The only difference noted so far is a slight elevation of brain Taurine levels. GAT1 and GAT3 have higher concentrations in the brain and have higher affinity to GABA. This makes them more likely than GAT2 to influence the activity of neurotransmitter GABA in the brain. Liver GAT2 is expressed in hepatocytes and is well positioned to take up GABA entering the liver from the intestine (via the portal vein), but it is not known if this is an important function. On the other hand, GAT2 is also able to transport taurine and it appears to be the major taurine transporter in the liver. Kidneys GAT2 is also present in proximal tubules in the kidney cortex, but only in the basolateral membranes. The physiological function is unknown. ==Clinical significance==

The clinical significance of GAT2 is at present undetermined. Some anticonvulsants have been reported to act upon the GABA transporters. There is evidence to suggest that GABA transporters are linked to epilepsy, affective disorders, and schizophrenia. But considering that GAT1 and GAT3 are expressed at far higher levels in brain tissue, it is likely that inhibition of these transporters will have a far greater anticonvulsant effect than inhibition of GAT2 ==References==