Tetrodotoxin-sensitive persistent current boosts the depolarization of retinal amacrine cells in goldfish
Tetrodotoxin-sensitive persistent current boosts the depolarization of retinal amacrine cells in goldfish
复制标题
河豚毒素敏感的持续电流促进金鱼视网膜无长突细胞的去极化
DOI：
10.1016/s0304-3940(99)00903-9
复制
发表时间：
2000
影响因子：
2.5
通讯作者：
A. Kaneko
中科院分区：
文献类型：
--
作者：
Shu;Hiromasa Satoh;A. Koizumi;T. Takayanagi;A. Kaneko
在光照条件下，视网膜无长突细胞呈渐进性去极化反应，并伴有棘波放电。一般认为，渐进性去极化是由双极细胞的兴奋性突触输入单独产生的。在这里，我们证明河豚毒素(TTX)敏感的持续电流也有助于梯度去极化。用全细胞膜片钳技术在制备的金鱼视网膜切片的无长突细胞中分离到这一电流。持续电流的激活阈值约为−50 mV，比黑暗中的膜电位高出约10 mV。因此，TTX敏感的持续电流很可能是无长突细胞兴奋性突触后电位的增强器。
To light illumination retinal amacrine cells respond with graded depolarization accompanied by a spike discharge. It has been assumed that the graded depolarization is produced solely by the excitatory synaptic inputs from bipolar cells. Here we demonstrate that a tetrodotoxin (TTX)-sensitive persistent current also contributes to the graded depolarization. This current was isolated in amacrine cells of the goldfish retinal slice preparations by the whole-cell patch clamp technique. The activation threshold of the persistent current was about −50 mV, approximately 10 mV more positive than the membrane potential in the dark. Therefore, it is highly likely that the TTX-sensitive persistent current is a booster of the excitatory postsynaptic potential in amacrine cells.