Lipton S A, Ostroy S E, Dowling J E
J Gen Physiol. 1977 Dec;70(6):747-70. doi: 10.1085/jgp.70.6.747.
The effects of altering extracellular Ca(2+) levels on the electrical and adaptive properties of toad rods have been examined. The retina was continually superfused in control (1.6 mM Ca(2+)) or test ringer's solutions, and rod electrical activity was recorded intracellularly. Low-calcium ringer's (10(-9)M Ca(2+)) superfused for up to 6 min caused a substantial depolarization of the resting membrane potential, an increase in light-evoked response amplitudes, and a change in the waveform of the light-evoked responses. High Ca(2+) ringer's (3.2 mM) hyperpolarized the cell membrane and decreased response amplitudes. However, under conditions of either low or high Ca(2+) superfusion for up to 6 min, in both dark-adapted and partially light-adapted states, receptor sensitivity was virtually unaffected; i.e., the V-log I curve for the receptor potential was always located on the intensity scale at a position predicted by the prevailing light level, not by Ca(2+) concentration. Thus, we speculate that cytosol Ca(2+) concentration is capable of regulating membrane potential levels and light-evoked response amplitudes, but not the major component of rod sensitivity. Low Ca(2+) ringer's also shortened the period of receptor response saturation after a bright but nonbleaching light flash, hence accelerating the onset of both membrane potential and sensitivity recovery during dark adaptation. Exposure of the retina to low Ca(2+) (10(-9)M) ringer's for long periods (7-15 min) caused dark-adapted rods to lose responsiveness. Response amplitudes gradually decreased, and the rods became desensitized. These severe conditions of low Ca(2+) caused changes in the dark-adapted rod that mimic those observed in rods during light adaptation. We suggest that loss of receptor sensitivity during prolonged exposure to low Ca(2+) ringer's results from a decrease of intracellular (intradisk) stores of Ca(2+); i.e., less Ca(2+) is thereby released per quantum catch.
研究了改变细胞外钙离子(Ca(2+))水平对蟾蜍视杆细胞电特性和适应性特性的影响。视网膜持续灌注对照(1.6 mM Ca(2+))或测试林格氏液,细胞内记录视杆细胞的电活动。低钙林格氏液(10(-9)M Ca(2+))灌注长达6分钟会导致静息膜电位大幅去极化、光诱发反应幅度增加以及光诱发反应波形改变。高钙林格氏液(3.2 mM)使细胞膜超极化并降低反应幅度。然而,在低钙或高钙灌注长达6分钟的条件下,无论是暗适应还是部分光适应状态,受体敏感性实际上未受影响;即,受体电位的V-log I曲线始终位于由当时光照水平预测的强度标度位置上,而非由Ca(2+)浓度决定。因此,我们推测胞质Ca(2+)浓度能够调节膜电位水平和光诱发反应幅度,但不是视杆细胞敏感性的主要组成部分。低钙林格氏液还缩短了明亮但非漂白光闪光后受体反应饱和的时间,从而加速了暗适应过程中膜电位和敏感性恢复的起始。将视网膜长时间(7 - 15分钟)暴露于低钙(10(-9)M)林格氏液会导致暗适应视杆细胞失去反应性。反应幅度逐渐降低,视杆细胞变得脱敏。这些低钙的严重条件导致暗适应视杆细胞发生的变化类似于光适应过程中视杆细胞所观察到的变化。我们认为,长时间暴露于低钙林格氏液期间受体敏感性的丧失是由于细胞内(盘内)Ca(2+)储存减少所致;即,每个量子捕获释放的Ca(2+)减少。