SNAT2 Amino Acid Transporter Is Regulated by Amino Acids of the SLC6 γ-Aminobutyric Acid Transporter Subfamily in Neocortical Neurons and May Play No Role in Delivering Glutamine for Glutamatergic Transmission

作者: Xiong Zhang , Stéphanie De Gois , Ali Shawki , Bryan Mackenzie , Chu Chen

DOI: 10.1074/JBC.M806470200

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摘要: System A transporters SNAT1 and SNAT2 mediate uptake of neutral α-amino acids (e.g. glutamine, alanine, proline) are expressed in central neurons. We tested the hypothesis that is required to support neurotransmitter glutamate synthesis by examining spontaneous excitatory activity after inducing or repressing expression for prolonged periods. stimulated de novo mRNA increased stability total protein functional activity, whereas was unaffected. Increased endogenous did not affect action-potential frequency over control. Long term glutamine exposure strongly repressed but frequency. Quantal size altered following induction repression. These results suggest glutamatergic transmission pyramidal neurons does rely on SNAT2. To our surprise, repression limited substrates. Taurine, γ-aminobutyric acid, β-alanine (substrates SLC6 acid transporter family) more potently (10×) than substrates; however, responses substrates were rapid. Since ATF4 (activating transcription factor 4) CCAAT/enhancer-binding known bind an amino response element within promoter peripheral cell lines, we whether either similarly induced deprivation found taurine both factors. Our data revealed constitutively low under physiological conditions induced, together with TauT, depletion acids.

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