Gotow T, Nishi T
Department of Physiology, School of Medicine, Kagoshima University, Japan.
Brain Res. 1991 Aug 23;557(1-2):121-8. doi: 10.1016/0006-8993(91)90124-e.
The internal messengers mediating the photocurrent of the molluscan extraocular photoreceptor, A-P-1, were examined. In the dark, pressure-injection of cGMP into the A-P-1, voltage-clamped at resting levels, produced a rapid outward current, associated with an increase in conductance. However, the cGMP-induced current and increase in conductance were suppressed by subsequent photostimulation, suggesting hydrolysis of cGMP by light. The steady-state I/V relation for the cGMP-induced current was non-linear. The I/V relation for the instantaneous cGMP-induced current, measured 50 ms after the beginning of a voltage step, was linear, and reversed at the membrane potential, -67 mV, which corresponded to the K+ equilibrium potential of A-P-1 in 10 mM K+ normal saline. These findings indicate that the internal cGMP induces a voltage- and time-dependent K+ current. Since the photocurrent results from the suppression of a voltage- and time-dependent K+ current similar to above, the photocurrent is considered to be equivalent to the suppression of the cGMP-induced current. Short pressure-injection of GDP-beta-S into A-P-1 reduced the subsequent photocurrent. The photocurrent was also suppressed after an external application of Pertussis toxin. On the other hand, the photocurrent was amplified by prior pressure-injection of inositol 1,4,5-trisphosphate (IP3). However, a short pressure-injection of neomycin into A-P-1 depressed the subsequent photocurrent. These results suggested that the cGMP-induced (dark) current is mediated by cGMP, and that hydrolysis of cGMP by light leads to the photocurrent, then being modified by another messenger, IP3, to be amplified.(ABSTRACT TRUNCATED AT 250 WORDS)
对介导软体动物眼外光感受器A-P-1光电流的细胞内信使进行了研究。在黑暗中,将cGMP压力注射到钳制在静息水平的A-P-1中,会产生快速外向电流,伴有电导增加。然而,cGMP诱导的电流和电导增加会被随后的光刺激所抑制,这表明cGMP被光水解。cGMP诱导电流的稳态I/V关系是非线性的。在电压阶跃开始后50毫秒测量的瞬时cGMP诱导电流的I/V关系是线性的,并在膜电位-67 mV处反转,该电位对应于10 mM K+生理盐水中A-P-1的K+平衡电位。这些发现表明细胞内cGMP诱导了一种电压和时间依赖性的K+电流。由于光电流是由类似于上述的电压和时间依赖性K+电流的抑制产生的,因此光电流被认为等同于cGMP诱导电流的抑制。向A-P-1中短暂压力注射GDP-β-S会降低随后的光电流。在外部应用百日咳毒素后,光电流也会被抑制。另一方面,预先向A-P-1中压力注射肌醇1,4,5-三磷酸(IP3)会放大光电流。然而,向A-P-1中短暂压力注射新霉素会抑制随后的光电流。这些结果表明,cGMP诱导的(暗)电流由cGMP介导,光对cGMP的水解导致光电流,然后由另一种信使IP3进行修饰以被放大。(摘要截短至250字)