When the retina of the toad, Bufo marinus, was superfused with 6-12 mM-tetraethylammonium chloride (TEA), intracellular recordings from rods showed large, depolarizing regenerative potentials. For brief exposures to TEA, these potentials occurred during the recovery phase of the light responses; whereas, during longer exposures, they were spontaneous in darkness but suppressed during illumination. Similar regenerative potentials were observed during perfusion with 3-10 mM-4-aminopyridine and 1-2 mM-BaCl2. 2. The amplitude of the regenerative potentials depended upon the extracellular Ca concentration ([Ca2+]o). Lowering [Ca2+]o decreased their amplitude and in zero [Ca2+]o they were reversibly abolished. Increasing [Ca2+]o by 1.5-2 times produced a small hyperpolarization of membrane potential and a large augmentation in regenerative response amplitude. However, larger increases in [Ca2+]o produced large membrane hyperpolarizations and reversibly suppressed the regenerative responses. 3. High concentrations of Sr2+ in TEA also enhanced regenerative activity but did not affect the rod resting membrane potential. The amplitude of regenerative potentials increased continuously with increasing [Sr2+]o, and in 28 mM-Sr2+ the rods generated 60-70 mV action potentials, even in the absence of extracellular Na+. 4. The regenerative potentials were blocked by 25 microM-Cd2+, 50-100 microM-Co2+, 5mM-Mg2+, and 100 microM-D-600. They were unaffected by 2 microM-TTX or 2-5 mM-Na aspartate. 5. In Ringer containing 12 mM-TEA, large anode break responses could be recorded from rods at the termination of inward current pulses. These anode break responses were also suppressed by Co2+ and unaffected by TTX or Na aspartate. 6. We conclude that the membrane of toad rods contains a conductance normally selective for Ca2+, which is activated by depolarization. In normal Ringer, the inward current through this conductance produces little effect, since it is balanced by a large outward current, probably carried by K+. TEA and other agents appear to block this outward current, permitting the Ca2+ current to become regenerative.
摘要
用6 - 12 mM氯化四乙铵(TEA)对海蟾蜍(Bufo marinus)的视网膜进行灌流时,对视杆细胞的细胞内记录显示出大的、去极化的再生电位。在短时间暴露于TEA时,这些电位出现在光反应的恢复阶段;而在长时间暴露期间,它们在黑暗中自发出现,但在光照时受到抑制。在用3 - 10 mM 4 - 氨基吡啶和1 - 2 mM氯化钡灌流期间也观察到类似的再生电位。2. 再生电位的幅度取决于细胞外钙浓度([Ca2+]o)。降低[Ca2+]o会降低其幅度,在零[Ca2+]o时它们会可逆地消失。将[Ca2+]o增加1.5 - 2倍会使膜电位产生小的超极化,并使再生反应幅度大幅增加。然而,[Ca2+]o的更大增加会导致大的膜超极化并可逆地抑制再生反应。3. TEA中高浓度的Sr2+也增强了再生活性,但不影响视杆细胞的静息膜电位。再生电位的幅度随着[Sr2+]o的增加而持续增加,在28 mM Sr2+时,即使在没有细胞外Na+的情况下,视杆细胞也能产生60 - 70 mV的动作电位。4. 再生电位被25 μM Cd2+、50 - 100 μM Co2+、5 mM Mg2+和100 μM D - 600阻断。它们不受2 μM TTX或2 - 5 mM天冬氨酸钠的影响。5. 在含有12 mM TEA的林格氏液中,在向内电流脉冲结束时可以从视杆细胞记录到大的阳极断电反应。这些阳极断电反应也被Co2+抑制,不受TTX或天冬氨酸钠的影响。6. 我们得出结论,蟾蜍视杆细胞膜含有一种通常对Ca2+有选择性的电导,它通过去极化被激活。在正常林格氏液中,通过这种电导的内向电流产生的影响很小,因为它被可能由K+携带的大的外向电流平衡。TEA和其他试剂似乎阻断了这种外向电流,使Ca2+电流能够产生再生。