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Effects of calcium and guanosine-35-cyclic-monophosphoric acid on receptor potentials of toad rods.

机译:钙和鸟苷35-环一磷酸对蟾蜍棒受体电位的影响。

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摘要

Membrane potential was recorded intracellularly from rod outer segments in the isolated retina of Bufo marinus. The composition of the solution flowing over the exposed receptor side of the retina was changed rapidly and ionophoretic injections were made into single rod outer segments. Lowering the external Ca2+ concentration, adding 3-isobutyl-1-methylxanthine (IBMX) to the bath, or ionophoretic injections of guanosine-3':5'-cyclic monophosphoric acid (cGMP) lead to depolarization of the rod membrane and an increase in the maximum peak amplitude of the receptor potential. Lowering the Ca2+ concentration or adding IBMX to the bath shifted the curve of response amplitude vs. long intensity of stimulus and sigma (intensity at half saturation) towards dimmer intensities. The ionophoresis of cGMP did not shift the position of the curve along the log stimulus intensity axis. Changing the external concentration of Ca or IBMX changes the form of the response amplitude vs. log intensity curve. This is most obvious at dim intensities. The amplitude of receptor potentials elicited by dim light was decreased by lowering Ca but increased by IBMX. The kinetics of receptor potentials were affected differently by solutions with a low Ca2+ concentration and those containing IBMX. The recovery phase of the receptor potential was slightly accelerated in the low Ca solution, whereas it was greatly slowed in the IBMX-containing solution. The ionophoretic injection of cGMP also slowed the recovery of the receptor potential. The data presented do not support the proposal that cGMP alone maintains membrane voltage in the dark and that the light-induced hydrolysis of cGMP results in the light-induced decrease in membrane conductance underlying the receptor potential. It is more likely that both Ca2+ and cGMP interact in the modulation of membrane voltage, perhaps as interrelated messengers.
机译:在蟾蜍海泡的离体视网膜中,从杆外段的细胞内记录膜电位。快速改变流过视网膜暴露的受体侧的溶液的组成,并将离子载体注射制成单杆外部段。降低外部Ca2 +浓度,在浴中添加3-异丁基-1-甲基黄嘌呤(IBMX),或离子注入鸟苷3':5'-环一磷酸(cGMP)导致杆膜去极化并增加杆状膜的极化。受体电位的最大峰值幅度。降低Ca2 +浓度或向浴中添加IBMX,会使响应幅度与长时间的刺激强度和sigma(半饱和强度)之间的关系曲线向较暗的强度方向移动。 cGMP的离子渗透法并没有沿着对数刺激强度轴移动曲线的位置。更改Ca或IBMX的外部浓度会更改响应幅度与对数强度曲线的形式。这在暗淡的强度下最明显。降低Ca可以降低昏暗光线引起的受体电位的幅度,而IBMX可以提高幅度。 Ca2 +浓度低的溶液和含IBMX的溶液对受体电位的动力学影响不同。在低钙溶液中,受体电势的恢复阶段略有加速,而在含IBMX的溶液中,受体电势的恢复阶段却大大减慢了。离子注射cGMP也减慢了受体电位的恢复。所提供的数据不支持cGMP仅在黑暗中维持膜电压并且光诱导的cGMP水解导致光诱导的受体电势下的膜电导降低的提议。 Ca2 +和cGMP更有可能在膜电压的调节中相互作用,也许是相互关联的信使。

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