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首页> 外文期刊>Neuron >Developmental Regulation and Activity-Dependent Maintenance of GABAergic Presynaptic Inhibition onto Rod Bipolar Cell Axonal Terminals
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Developmental Regulation and Activity-Dependent Maintenance of GABAergic Presynaptic Inhibition onto Rod Bipolar Cell Axonal Terminals

机译：杆双极细胞轴突末端的GABA能突触前抑制的发展调节和活性依赖维持。

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Presynaptic inhibition onto axons regulates neuronal output, but how such inhibitory synapses develop and are maintained in vivo remains unclear. Axon terminals of glutamatergic retinal rod bipolar cells (RBCs) receive GABAA and GABAC receptor-mediated synaptic inhibition. We found that perturbing GABAergic or glutamatergic neurotransmission does not prevent GABAergic synaptogenesis onto RBC axons. But, GABA release is necessary for maintaining axonal GABA receptors. This activity-dependent process is receptor subtype specific: GABAC receptors are maintained, whereas GABAA receptors containing α1, but not α3, subunits decrease over time in mice with deficient GABA synthesis. GABAA receptor distribution on RBC axons is unaffected in GABAC receptor knockout mice. Thus, GABAA and GABAC receptor maintenance are regulated separately. Although immature RBCs elevate their glutamate release when GABA synthesis is impaired, homeostatic mechanisms ensure that the RBC output operates within its normal range after eye opening, perhaps to regain proper visual processing within the scotopic pathway. Schubert et al. show that GABAergic transmission regulates maintenance of GABA receptors on retinal axon terminals in a receptor subtype-specific manner.
机译：突触前对轴突的抑制作用可调节神经元输出，但尚不清楚这种抑制性突触如何在体内形成和维持。谷氨酸能视网膜视杆双极细胞（RBC）的轴突末端接受GABAA和GABAC受体介导的突触抑制。我们发现扰动GABA能或谷氨酸能神经传递并不能阻止RABA轴突上GABA能的突触发生。但是，GABA的释放对于维持轴突GABA受体是必需的。这种依赖于活性的过程是受体亚型特异性的：GABAC受体得以维持，而GABA合成不足的小鼠中，含有α1但不包含α3亚基的GABAA受体会随时间减少。 RBC轴突上的GABA A受体分布在GABA C受体敲除小鼠中不受影响。因此，GABAA和GABAC受体的维持是分开调节的。尽管当GABA合成受损时，未成熟的RBC会增加其谷氨酸的释放，但体内平衡机制可确保在睁开眼睛后RBC的输出在其正常范围内运行，也许可以在暗视途径中恢复正常的视觉处理。舒伯特等。表明GABA能传递以受体亚型特异性方式调节视网膜轴突末端GABA受体的维持。

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