GABA-Induced intrinsic light-scattering changes associated with voltage-sensitive dye signals in embryonic brain stem slices: coupling of depolarization and cell shrinkage.
GABA-Induced intrinsic light-scattering changes associated with voltage-sensitive dye signals in embryonic brain stem slices: coupling of depolarization and cell shrinkage.
复制标题
GABA 诱导的与胚胎脑干切片中电压敏感染料信号相关的内在光散射变化：去极化和细胞收缩的耦合。
作者：
Y. Momose;Katsushige Sato;A. Hirota;K. Kamino
我们发现了新的证据，γ-氨基丁酸（GABA）诱导的内在光学变化与电压敏感的染料信号在早期胚胎鸡脑干切片。从8天大的胚胎制备切片，并用电压敏感染料（NK 2761）对它们进行染色。压力喷射GABA的一个网站内的准备引起光学变化。用580 nm的入射光，两个组件被确定在GABA诱导的光学变化。第一个分量是波长相关的，而第二个，较慢的变化是独立的波长。与已知的染料的作用光谱的比较表明，第一个组件反映了一个去极化的膜和第二个，缓慢的组件是光散射的变化，从细胞收缩耦合的去极化。类似的光学变化也引起甘氨酸，虽然幅度的第一和第二个信号是远远小于GABA。GABA诱导的光学变化持续存在的印防己毒素和2-羟基苯甲酸，这表明这些光学响应包括一个新的GABA的反应，这已被称为GABAD在我们以前的报告。
We have found new evidence for gamma-aminobutyric acid (GABA)-induced intrinsic optical changes associated with a voltage-sensitive dye signal in the early embryonic chick brain stem slice. The slices were prepared from 8-day-old embryos, and they were stained with a voltage-sensitive dye (NK2761). Pressure ejection of GABA to one site within the preparation elicited optical changes. With 580-nm incident light, two components were identified in the GABA-induced optical change. The first component was wavelength dependent, whereas the second, slower change was independent of wavelength. Comparison with the known action spectrum of the dye indicates that the first component reflects a depolarization of the membrane and that the second, slow component is a light-scattering change resulting from cell shrinkage coupled with the depolarization. Similar optical changes also were induced by glycine, although the amplitude of both the first and second signals was much smaller than for GABA. The optical changes induced by GABA persisted in the presence of picrotoxin and 2-hydroxysaclofen, suggesting that these optical responses include a novel GABA response, which has been termed GABAD in our previous reports.
影响因子：
56.9
作者：
MCBAIN, CJ;TRAYNELIS, SF;DINGLEDINE, R
通讯作者：
DINGLEDINE, R