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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >GABA uptake into astrocytes is not associated with significant metabolic cost: Implications for brain imaging of inhibitory transmission.
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GABA uptake into astrocytes is not associated with significant metabolic cost: Implications for brain imaging of inhibitory transmission.

机译：星形胶质细胞摄取GABA与显着的代谢成本无关：抑制性传播对脑部成像的影响。

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摘要

Synaptically released glutamate has been identified as a signal coupling excitatory neuronal activity to increased glucose utilization. The proposed mechanism of this coupling involves glutamate uptake into astrocytes resulting in increased intracellular Na+ (Nai+) and activation of the Na+/K+-ATPase. Increased metabolic demand linked to disruption of Nai+ homeostasis activates glucose uptake and glycolysis in astrocytes. Here, we have examined whether a similar neurometabolic coupling could operate for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), also taken up by Na+-dependent transporters into astrocytes. Thus, we have compared the Nai+ response to GABA and glutamate in mouse astrocytes by microspectrofluorimetry. The Nai+ response to GABA consisted of a rapid rise of 4-6 mM followed by a plateau that did not, however, significantly activate the pump. Indeed, the GABA transporter-evoked Na+ influxes are transient in nature, almost totally shutting off within approximately 30 sec ofGABA application. The metabolic consequences of the GABA-induced Nai+ response were evaluated by monitoring cellular ATP changes indirectly in single cells and measuring 2-deoxyglucose uptake in astrocyte populations. Both approaches showed that, whereas glutamate induced a robust metabolic response in astrocytes (decreased ATP levels and glucose uptake stimulation), GABA did not cause any measurable metabolic response, consistent with the Nai+ measurements. Results indicate that GABA does not couple inhibitory neuronal activity with glucose utilization, as does glutamate for excitatory neurotransmission, and suggest that GABA-mediated synaptic transmission does not contribute directly to brain imaging signals based on deoxyglucose.
机译：突触释放的谷氨酸已被鉴定为将兴奋性神经元活性与葡萄糖利用增加耦合的信号。提出的这种偶联机制涉及谷氨酸摄取到星形胶质细胞中，导致细胞内Na +（Nai +）增加和Na + / K + -ATPase活化。与Nai +动态平衡破坏有关的新陈代谢需求增加，激活星形胶质细胞中的葡萄糖摄取和糖酵解。在这里，我们检查了类似的神经代谢偶联是否可以对抑制性神经递质γ-氨基丁酸（GABA）起作用，其也被依赖Na +的转运蛋白吸收到星形胶质细胞中。因此，我们通过荧光光谱法比较了小鼠星形胶质细胞对GABA和谷氨酸的Nai +反应。 Nai +对GABA的反应包括4-6 mM的快速升高，随后是平台期，但没有明显激活泵。实际上，GABA转运蛋白诱发的Na +流入本质上是短暂的，在施用GABA的大约30秒内几乎完全关闭。通过间接监测单个细胞中细胞ATP的变化并测量星形胶质细胞群体中2-脱氧葡萄糖的摄取，来评估GABA诱导的Nai +反应的代谢后果。两种方法均表明，尽管谷氨酸诱导星形胶质细胞发生强烈的代谢反应（ATP水平降低和葡萄糖摄取刺激降低），但与Nai +测量结果一致，GABA并未引起任何可测量的代谢反应。结果表明，GABA不会将抑制性神经元活动与葡萄糖利用耦合在一起，谷氨酸对兴奋性神经传递也没有影响，并且表明GABA介导的突触传递不会直接促进基于脱氧葡萄糖的脑成像信号。

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