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首页> 外文期刊>The European Journal of Neuroscience >Calcium-dependent inactivation and depletion of synaptic cleft calcium ions combine to regulate rod calcium currents under physiological conditions.
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Calcium-dependent inactivation and depletion of synaptic cleft calcium ions combine to regulate rod calcium currents under physiological conditions.

机译：钙依赖的失活和突触裂隙钙离子的消耗结合起来，在生理条件下调节杆的钙电流。

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L-type Ca2+ currents (ICa) in rod photoreceptors exhibit Ca2+-dependent inactivation. Perforated-patch whole-cell recordings were obtained from isolated rods of the tiger salamander using 1.8 mm Ca2+ in the bathing medium to determine the extent of Ca2+-dependent inactivation of ICa with physiological [Ca2+] and endogenous buffering. ICa was measured with voltage ramps applied before and after 5-s steps to -40, -30, -20, or -10 mV. Long depolarizing steps in isolated rods produced inactivation of ICa ranging from 15% at -40 mV to > 80% at -10 mV. Because, in addition to Ca2+-dependent inactivation, depletion of synaptic cleft Ca2+ accompanying activation of ICa can reduce presynaptic ICa at calycal synapses, we investigated whether a similar mechanism worked at the invaginating rod synapse. Rods from retinal slices with intact synapses were compared with isolated rods in which synaptic cleft depletion is absent. ICa was more strongly depressed by depolarization of rods in retinal slices, with ICa reduced by 47% following voltage steps to -40 mV. The depression of currents by depolarization was also greater for rods from retinal slices than isolated rods when Ca2+ was replaced with Ba2+ to reduce Ca2+-dependent inactivation. The stronger depolarization-evoked inhibition of ICa in retinal slices compared to isolated rods probably reflects depletion of synaptic cleft Ca2+ arising from sustained Ca2+ influx. Inactivation of ICa exhibited slow onset and recovery. These findings suggest that Ca2+-dependent inactivation and depletion of synaptic cleft Ca2+ may combine to regulate ICa in response to light-evoked changes in rod membrane potential.
机译：棒状光感受器中的L型Ca2 +电流（ICa）表现出Ca2 +依赖性失活。从虎sal的分离棒中获得穿孔的全细胞记录，使用沐浴介质中的1.8 mm Ca2 +来确定具有生理[Ca2 +]和内源缓冲作用的ICa的Ca2 +依赖性失活程度。通过在5 s步之前和之后施加电压斜坡至-40，-30，-20或-10 mV来测量ICa。隔离棒中的长去极化步骤导致ICa失活，范围从-40 mV的15％到-10 mV的> 80％。因为，除了依赖Ca2 +的失活外，伴随ICa激活的突触间隙Ca2 +的耗竭还可以减少大耳突触中的突触前ICa，因此我们研究了类似的机制在渐进的杆突触中是否起作用。将具有完整突触的视网膜切片的视杆与不存在突触裂隙耗竭的孤立视杆进行比较。视网膜切片中棒的去极化使ICa受到更强烈的抑制，电压阶跃降至-40 mV后ICa降低了47％。当用Ba2 +代替Ca2 +以减少Ca2 +依赖性失活时，来自视网膜切片的棒的去极化电流抑制也比分离的棒大。与分离的棒相比，视网膜切片中对ICa的去极化诱发的抑制作用更强，这可能反映了持续的Ca2 +流入引起的突触性裂隙Ca2 +的消耗。 ICa的失活表现出缓慢的发作和恢复。这些发现表明，Ca2 +依赖的失活和突触裂痕Ca2 +的耗竭可能结合调节ICa来响应杆状膜电位的光诱发变化。

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