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.

中文翻译：

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谷氨酰胺转运蛋白Slc38a1调节GABA能神经传递和突触可塑性。

从神经系统发育到种群活动和突触可塑性的同步化，GABA信号维持了大脑的基本功能。尽管具有这些关键特征，但强调囊泡神经递质GABA的快速和细胞自主补充及其对突触可塑性的影响的分子决定因素仍然难以捉摸。在这里，我们表明，小鼠中谷氨酰胺转运蛋白Slc38a1的遗传破坏阻碍了GABA的合成，修饰了GABA能突触前突触囊泡的形态，并损害了关键时期的可塑性。我们证明，Slc38a1介导的谷氨酰胺运输调节水泡GABA含量，诱导高频膜振荡，并塑造皮层加工和可塑性。在一起