Glutamine is an astroglia-derived precursor of the neurotransmitter glutamate, and its astroglia-to-neuron transfer is controlled by distinct glutamine transporters on the astrocytic and neuronal sites. In this study, we focused on the role of astrocytic glutamine efflux-mediating system N transporter SN1 in the maintenance of glutamatergic neurotransmission by analyzing the electrophysiological parameters ex vivo in the brain slices from control mice and mice in which vivo-morpholino technique was used to diminish SN1 protein. The glutamatergic transmission was characterized by electrophysiological recordings, ultrastructure of neuron terminals, and determination of proteins related to glutamate synaptic transmission: synaptophysin, synaptotagmin, and vit1A. The space-restricted ∼51,5% reduction of SN1 protein did not affect the expression of the neuronal glutamine transporter SAT2. SN1 depletion resulted in a reduction of field potentials (FPs), unaltered frequency of spontaneous and miniature excitatory postsynaptic currents (sEPSCs/mEPSCs), and presented a tendency towards a decrease of long-term potentiation (LTP). Ultrastructurally, preserved number of synaptic vesicles, primarily localized centrally of the cell body, correlates with unchanged levels of synaptic proteins. Collectively, the study indicates that glutamatergic transmission proceeds relatively independently of the SN1 - mediated glutamine transfer to the synapse.

谷氨酰胺是神经递质谷氨酸的一种源自星形胶质细胞的前体，其星形胶质细胞向神经元的转移受星形胶质细胞和神经元部位上独特的谷氨酰胺转运蛋白的控制。在这项研究中，我们通过分析离体的电生理参数，重点研究了星形细胞谷氨酰胺外流介导系统N转运蛋白SN1在维持谷氨酸能神经传递中的作用。对照小鼠和使用体内吗啉代技术来减少SN1蛋白的小鼠的脑切片中的蛋白质。谷氨酸能传递的特征在于电生理学记录，神经元末端的超微结构以及与谷氨酸突触传递有关的蛋白质的测定：突触素，突触标记素和vit1A。SN1蛋白的空间限制减少了约51.5％，这并不影响神经元谷氨酰胺转运蛋白SAT2的表达。SN1耗竭导致场电位（FPs）减少，自发和微型兴奋性突触后电流（sEPSCs / mEPSCs）的频率不变，并呈现出长期增强（LTP）降低的趋势。超微结构，保留的突触小泡数量主要位于细胞体的中央，与突触蛋白水平不变相关。总体而言，该研究表明，谷氨酸能传递相对独立于SN1介导的谷氨酰胺转移到突触。