@article {64904,
	title = {The glutamine transporter Slc38a1 regulates GABAergic neurotransmission and synaptic plasticity.},
	journal = {Cerebal Cortex},
	year = {2019},
	month = {2019 May 03},
	abstract = {<p>GABA signaling sustains fundamental brain functions, from nervous system development to the synchronization of population activity and synaptic plasticity. Despite these pivotal features, molecular determinants underscoring the rapid and cell-autonomous replenishment of the vesicular neurotransmitter GABA and its impact on synaptic plasticity remain elusive. Here, we show that genetic disruption of the glutamine transporter Slc38a1 in mice hampers GABA synthesis, modifies synaptic vesicle morphology in GABAergic presynapses and impairs critical period plasticity. We demonstrate that Slc38a1-mediated glutamine transport regulates vesicular GABA content, induces high-frequency membrane oscillations and shapes cortical processing and plasticity. Taken together, this work shows that Slc38a1 is not merely a transporter accumulating glutamine for metabolic purposes, but a key component regulating several neuronal functions.</p>
},
	issn = {1460-2199},
	doi = {10.1093/cercor/bhz055},
	author = {Qureshi, Tayyaba and S{\o}rensen, Christina and Berghuis, Paul and Jensen, Vidar and Dobszay, Marton B and Farkas, Tam{\'a}s and Dalen, Knut Tomas and Guo, Caiying and Hassel, Bj{\o}rnar and Utheim, Tor Paaske and Hvalby, {\O}ivind and Hafting, Torkel and Harkany, Tibor and Fyhn, Marianne and Chaudhry, Farrukh Abbas}
}
@article {6922,
	title = {Deletion of the γ-aminobutyric acid transporter 2 (GAT2 and SLC6A13) gene in mice leads to changes in liver and brain taurine contents.},
	journal = {The Journal of Biological Chemistry},
	volume = {287},
	year = {2012},
	month = {2012 Oct 12},
	pages = {35733-46},
	abstract = {<p>The GABA transporters (GAT1, GAT2, GAT3, and BGT1) have mostly been discussed in relation to their potential roles in controlling the action of transmitter GABA in the nervous system. We have generated the first mice lacking the GAT2 (slc6a13) gene. Deletion of GAT2 (both mRNA and protein) neither affected growth, fertility, nor life span under nonchallenging rearing conditions. Immunocytochemistry showed that the GAT2 protein was predominantly expressed in the plasma membranes of periportal hepatocytes and in the basolateral membranes of proximal tubules in the renal cortex. This was validated by processing tissue from wild-type and knockout mice in parallel. Deletion of GAT2 reduced liver taurine levels by 50\%, without affecting the expression of the taurine transporter TAUT. These results suggest an important role for GAT2 in taurine uptake from portal blood into liver. In support of this notion, GAT2-transfected HEK293 cells transported [(3)H]taurine. Furthermore, most of the uptake of [(3)H]GABA by cultured rat hepatocytes was due to GAT2, and this uptake was inhibited by taurine. GAT2 was not detected in brain parenchyma proper, excluding a role in GABA inactivation. It was, however, expressed in the leptomeninges and in a subpopulation of brain blood vessels. Deletion of GAT2 increased brain taurine levels by 20\%, suggesting a taurine-exporting role for GAT2 in the brain.</p>
},
	keywords = {Animals, Brain, Brain Chemistry, GABA Plasma Membrane Transport Proteins, HEK293 Cells, Hepatocytes, Humans, Kidney Cortex, Kidney Tubules, Knockout, Liver, Male, Mice, Proximal, Rabbits, Rats, Taurine, Wistar},
	issn = {1083-351X},
	doi = {10.1074/jbc.M112.368175},
	author = {Zhou, Yun and Holmseth, Silvia and Guo, Caiying and Hassel, Bj{\o}rnar and H{\"o}fner, Georg and Huitfeldt, Henrik S and Wanner, Klaus T and Danbolt, Niels C}
}
