Calcium-induced calcium release in rod photoreceptor terminals boosts synaptic transmission during maintained depolarization
Calcium-induced calcium release in rod photoreceptor terminals boosts synaptic transmission during maintained depolarization
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DOI：
10.1111/j.1460-9568.2006.04845.x
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发表时间：
2006-06-01
影响因子：
3.4
通讯作者：
Thoreson, Wallace B.
中科院分区：
文献类型：
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作者：
Cadetti, Lucia;Bryson, Eric J.;Thoreson, Wallace B.
我们研究了钙诱导的钙释放(CICR)在杆状感光细胞终末突触传递中的作用。全细胞记录和共聚焦钙成像实验在含有完整突触终末的杆状突触上进行。低浓度的兰诺定刺激视杆细胞终末钙增加，这与兰诺定受体的存在一致。施加持续时间超过200ms或更长时间的强去极化步骤(-70至-10 mV)，可诱发一波钙波，并蔓延至电压钳制视杆的突触终末。这种继发性钙升高被高浓度的兰尼定所阻断，表明这是由于CICR引起的。兰尼定(50 MU M)对视杆细胞钙电流(i-ca)无明显影响，但对视杆细胞的光诱发电压反应有轻微的抑制作用。50 mU M兰诺定浴对水平细胞的光诱发电流有强烈的抑制作用。无论是细胞外应用还是通过膜片吸管进入视杆细胞，兰诺定(50mM)也可通过使视杆细胞去极化而抑制水平细胞中诱发的兴奋性突触后电流(EPSCs)。Ryanodine使去极化步长为200ms或更长的EPSCs的后期部分优先减少。这些结果表明，CICR增强了持续去极化引起的视杆细胞终末钙的增加，进而促进了视杆细胞的突触胞吐。
We examined the contribution of calcium-induced calcium release (CICR) to synaptic transmission from rod photoreceptor terminals. Whole-cell recording and confocal calcium imaging experiments were conducted on rods with intact synaptic terminals in a retinal slice preparation from salamander. Low concentrations of ryanodine stimulated calcium increases in rod terminals, consistent with the presence of ryanodine receptors. Application of strong depolarizing steps (-70 to -10 mV) exceeding 200 ms or longer in duration evoked a wave of calcium that spread across the synaptic terminals of voltage-clamped rods. This secondary calcium increase was blocked by high concentrations of ryanodine, indicating it was due to CICR. Ryanodine (50 mu M) had no significant effect on rod calcium current (I-ca) although it slightly diminished rod light-evoked voltage responses. Bath application of 50 mu M ryanodine strongly inhibited light-evoked currents in horizontal cells. Whether applied extracellularly or delivered into the rod cell through the patch pipette, ryanodine (50 mu M) also inhibited excitatory post-synaptic currents (EPSCs) evoked in horizontal cells by depolarizing steps applied to rods. Ryanodine caused a preferential reduction in the later portions of EPSCs evoked by depolarizing steps of 200 ms or longer. These results indicate that CICR enhances calcium increases in rod terminals evoked by sustained depolarization, which in turn acts to boost synaptic exocytosis from rods.