Reciprocal interactions between calcium and chloride in rod photoreceptors.
Reciprocal interactions between calcium and chloride in rod photoreceptors.
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DOI：
10.1152/jn.00932.2002
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发表时间：
2003-09
影响因子：
2.5
通讯作者：
W. Thoreson;E. J. Bryson;K. Rábl
中科院分区：
文献类型：
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作者：
W. Thoreson;E. J. Bryson;K. Rábl
本研究使用成像和电生理技术在蝾螈视网膜切片中关联视杆细胞中的Ca 2+和Cl-水平，从而检验Ca 2+和Ca 2+激活的Cl-通道之间的反馈相互作用的假设，由此Cl-通过Cl-通道流出可以抑制Ca 2+通道。增加[K +] o水平产生了浓度依赖性去极化的杆伴随着增加[Ca2 +] i与Fura-2测量。将[Ca 2 +] i增加的电压依赖性与钙电流（ICa）的电压依赖性进行比较。[Cl-] i用染料MEQ测量。高K+至低于-20 mV的膜电位的去极化降低[Cl-] i;较大的去极化增加[Cl-] i。Na/K/Cl共转运抑制剂布美他尼使表观Cl-平衡电位（ECl）向更负的电位移动，表明该共转运蛋白有助于建立相对去极化的ECl。由高K+诱发的MEQ荧光变化被尼氟灭酸（0.1 mM）、NPPB（2 μ M）或用Ba 2+替代Ca 2+抑制，表明去极化诱发的Cl-变化部分来自Ca 2+激活的Cl-通道的刺激。用CH3SO4-替代>/= 12 mM [Cl-] o可显著降低[Cl-] i。[Ca2用CH_3SO_4~-代替>/= 12 mM [Cl~-] o也能显著抑制20或50 mM K~+引起的[Cl~-] i增加。因此，适度的去极化可以引起[Ca2 +] i的增加，导致[Cl-] i的减少，相反，[Cl-] i的减少抑制去极化引起的[Ca2 +] i增加。这些发现支持了这样的假设，即Ca~（2+）和Ca~（2+）激活的Cl~-通道之间的反馈相互作用可能有助于调节突触前Ca~（2+）电流参与视杆细胞的突触传递。
This study used imaging and electrophysiological techniques in salamander retinal slices to correlate Ca2+ and Cl- levels in rods and thus test the hypothesis of a feedback interaction between Ca2+- and Ca2+-activated Cl- channels whereby Cl- efflux through Cl- channels can inhibit Ca2+ channels. Increasing [K+]o levels produced a concentration-dependent depolarization of rods accompanied by increases in [Ca2+]i measured with Fura-2. The voltage dependence of increases in [Ca2+]i was compared with the voltage dependence of the calcium current (ICa). [Cl-]i was measured with the dye, MEQ. Depolarization with high K+ to membrane potentials below -20 mV reduced [Cl-]i; larger depolarizations increased [Cl-]i. The Na/K/Cl cotransport inhibitor, bumetanide, shifted the apparent Cl- equilibrium potential (ECl) to more negative potentials, suggesting that this cotransporter helps establish a relatively depolarized ECl. MEQ fluorescence changes evoked by high K+ were inhibited by niflumic acid (0.1 mM), NPPB (2 microM), or replacement of Ca2+ with Ba2+, suggesting that depolarization-evoked Cl- changes result partly from stimulation of Ca2+-activated Cl- channels. Replacing >/=12 mM [Cl-]o with CH3SO4- produced a significant reduction in [Cl-]i. [Ca2+]i increases evoked by 20 or 50 mM K+ were also significantly inhibited by replacing >/=12 mM [Cl-]o with CH3SO4-. Thus modest depolarization can evoke increases in [Ca2+]i that lead to reductions in [Cl-]i, and conversely, reductions in [Cl-]i inhibit depolarization-evoked [Ca2+]i increases. These findings support the hypothesis that feedback interactions between Ca2+- and Ca2+-activated Cl- channels may contribute to the regulation of presynaptic Ca2+ currents involved in synaptic transmission from rod photoreceptors.