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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CONE PHOTORECEPTORS RESPOND TO THEIR OWN GLUTAMATE RELEASE IN THE TIGER SALAMANDER
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CONE PHOTORECEPTORS RESPOND TO THEIR OWN GLUTAMATE RELEASE IN THE TIGER SALAMANDER

机译：响应它们自身的谷氨酸释放的锥体光感受器

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Pulse-like currents resembling miniature postsynaptic currents were recorded in patch-clamped isolated cones from the tiger salamander retina, The events were absent in isolated cones without synaptic terminals, The frequency of events was increased by either raising the osmotic pressure or depolarizing the cell. It was decreased by the application of either glutamate or the glutamate-transport blockers dihydrokainate and D,L-threo-3-hydroxyaspartate, The events required external Na+ for which Li+ could not substitute. The reversal potential of these currents followed the equilibrium potential for Cl- when internal Cl- concentration was changed. Thus, these miniature currents appear to represent the presynaptic activation of the glutamate receptor with glutamate transporter-like pharmacology, caused by the photoreceptor's own vesicular glutamate release, Using a noninvasive method to preserve the intracellular Cl- concentration, we showed that glutamate elicits an outward current in isolated cones, Fluorescence of the membrane-permeable form of fura-2 was used to monitor Ca2+ entry at the cone terminal as a measure of membrane depolarization, The increase in intracellular Ca2+ concentration, elicited by puff application of 30 mM KCI, was completely suppressed in the presence of 100 mu M glutamate. Puff application of glutamate alone had no measurable depolarizing effect, These results suggest that the equilibrium potential for Cl-, E(CI), was more negative than the activation range for Ca2+ channels and that glutamate elicited an outward current, hyperpolarizing the cones. [References: 28]
机译：在来自虎sal视网膜的膜片钳隔离视锥中记录了类似于微型突触后电流的脉冲状电流。在无突触末端的隔离视锥中不存在该事件。通过增加渗透压或使细胞去极化来增加事件的发生频率。通过使用谷氨酸盐或谷氨酸盐转运阻滞剂二氢海藻酸盐和D，L-苏-3-羟基天冬氨酸盐可以降低这种情况。这些事件需要外部Na +，而Li +不能替代。当内部Cl-浓度改变时，这些电流的反向电位跟随Cl-的平衡电位。因此，这些微小电流似乎代表了谷氨酸转运蛋白样药理作用对谷氨酸受体的突触前激活，这是由于感光体自身的囊泡谷氨酸释放引起的。使用非侵入性方法保持细胞内Cl-浓度，我们证明了谷氨酸引起了向外在分离的视锥细胞中，电流通过Fura-2的膜渗透性形式的荧光来监测视锥末端的Ca2 +进入，以作为膜去极化的量度，通过抽吸30 mM KCI引起的细胞内Ca2 +浓度的增加为在100μM谷氨酸的存在下被完全抑制。单用谷氨酸粉扑就没有可测量的去极化作用。这些结果表明，Cl-，E（CI）的平衡电位比Ca2 +通道的激活范围更负，谷氨酸激发出向外的电流，使视锥细胞超极化。 [参考：28]

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