Ayoub G S, Lam D M
Center for Biotechnology, Cullen Eye Institute and Program in Neuroscience, Baylor College of Medicine, Houston, TX 77030.
Vision Res. 1987;27(12):2027-34. doi: 10.1016/0042-6989(87)90117-9.
In the goldfish retina, H1 horizontal cells, which receive input predominantly from red sensitive cone photoreceptors, possess a single high-affinity uptake mechanism for gamma-aminobutyric acid (GABA). This GABA uptake is enhanced by light stimulation, which hyperpolarizes the H1 cells. The regulation of this uptake mechanism was examined in isolated horizontal cells by measuring the accumulation of exogenously supplied 3H-GABA. Solutions containing elevated external K+ or glutamate were used to quantitatively depolarize the cells to reveal that the potential-sensitive GABA uptake is maximal under hyperpolarizing conditions and minimal with depolarization. The driving force for GABA uptake is derived from the Na+ electrochemical gradient, with approximately 2 Na+ ions being cotransported with each molecule of GABA. The results presented suggest that the uptake mechanism permits the synaptic concentration of GABA to be regulated by the membrane potential of the H1 horizontal cells. This, then permits the presynaptic horizontal cell to modulate the synaptic concentration of transmitter in this tonically active synapse.
在金鱼视网膜中,H1水平细胞主要接收来自红色敏感视锥光感受器的输入,它具有一种单一的高亲和力γ-氨基丁酸(GABA)摄取机制。这种GABA摄取通过光刺激增强,光刺激会使H1细胞超极化。通过测量外源供应的3H-GABA的积累,在分离的水平细胞中研究了这种摄取机制的调节。含有升高的细胞外K+或谷氨酸的溶液用于使细胞定量去极化,以揭示电位敏感的GABA摄取在超极化条件下最大,而去极化时最小。GABA摄取的驱动力来自Na+电化学梯度,每分子GABA大约有2个Na+离子协同转运。所呈现的结果表明,摄取机制允许GABA的突触浓度受H1水平细胞膜电位调节。这进而允许突触前水平细胞调节这个持续活动突触中递质的突触浓度。