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γ-氨基丁酸、甘氨酸及其拮抗剂对非洲爪蟾视网膜水平细胞的作用。

The actions of gamma-aminobutyric acid, glycine and their antagonists upon horizontal cells of the Xenopus retina.

作者信息

Stone S, Witkovsky P

出版信息

J Physiol. 1984 Aug;353:249-64. doi: 10.1113/jphysiol.1984.sp015334.

Abstract

We examined the effects of gamma-aminobutyric acid (GABA) and glycine and their respective antagonists, picrotoxin and strychnine, upon the membrane potential and light-evoked responses of the type H1 horizontal cell of the Xenopus retina. This horizontal cell receives mixed input from rod and cone receptors. Under control conditions the mean membrane potential was -37.8 +/- 9.7 mV. Addition of 5 mM-GABA to the superfusate hyperpolarized the cell by 4.0 +/- 2.6 mV within 3-5 min; addition of 0.5 mM-picrotoxin depolarized the cell by 4.3 +/- 2.1 mV. Prolonged (greater than 15 min) exposures to the drugs elicited more pronounced changes in membrane potential. GABA and picrotoxin affected primarily the cone-dependent input to the H1 horizontal cell. Under dark-adapted conditions, response wave forms were essentially unaltered by the drugs, but when the horizontal cell was moderately or fully light adapted, GABA reduced and picrotoxin enhanced the cone-dependent component of its response to light. Long-term (greater than 15 min) exposures to GABA and picrotoxin elicited changes in response kinetics usually associated with dark and light adaptation, respectively. Glycine, at bath concentrations of 0.6 mM or greater, depolarized horizontal cells by 21 mV on average and reduced or abolished their light response. This action did not occur in the presence of 0.1 mM-strychnine. When all light-evoked activity was blocked by 20-40 mM-magnesium, the depolarizing action of glycine still occurred. Thus, glycine appears to act directly upon the horizontal cell membrane. Neither GABA nor glycine, nor their respective antagonists, affected the spatial extent of the horizontal cell receptive field.

摘要

我们研究了γ-氨基丁酸(GABA)和甘氨酸及其各自的拮抗剂印防己毒素和士的宁对非洲爪蟾视网膜H1型水平细胞的膜电位和光诱发反应的影响。这种水平细胞接收来自视杆和视锥感受器的混合输入。在对照条件下,平均膜电位为-37.8±9.7 mV。向灌流液中添加5 mM - GABA在3 - 5分钟内使细胞超极化4.0±2.6 mV;添加0.5 mM印防己毒素使细胞去极化4.3±2.1 mV。长时间(大于15分钟)暴露于这些药物会引起膜电位更明显的变化。GABA和印防己毒素主要影响H1水平细胞的视锥依赖性输入。在暗适应条件下,药物基本不改变反应波形,但当水平细胞处于中度或完全光适应状态时,GABA会降低而印防己毒素会增强其对光的视锥依赖性反应成分。长时间(大于15分钟)暴露于GABA和印防己毒素分别引起通常与暗适应和光适应相关的反应动力学变化。甘氨酸在浴液浓度为0.6 mM或更高时,平均使水平细胞去极化21 mV,并降低或消除其光反应。在存在0.1 mM士的宁时,这种作用不会发生。当所有光诱发活动被20 - 40 mM镁阻断时,甘氨酸的去极化作用仍然会出现。因此,甘氨酸似乎直接作用于水平细胞膜。GABA、甘氨酸及其各自的拮抗剂均不影响水平细胞感受野的空间范围。

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