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首页> 外文期刊>The Journal of Physiology >Intracellular calcium reduces light-induced excitatory post-synaptic responses in salamander retinal ganglion cells.
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Intracellular calcium reduces light-induced excitatory post-synaptic responses in salamander retinal ganglion cells.

机译：细胞内钙可减少sal视网膜神经节细胞中光诱导的兴奋性突触后反应。

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摘要

The whole-cell patch clamp technique was used to study the effect of intracellular Ca2+ on light-evoked EPSCs in on-off ganglion cells in salamander retinal slices. Both AMPA and NMDA receptors contributed to the light-evoked responses. In the presence of strychnine and picrotoxin, ganglion cells responded to light onset and offset with transient inward currents at -70 mV. These currents were reduced by 35 +/- 3 % when the light stimulus was preceded by a depolarizing step from -70 to 0 mV. The inhibitory effect of depolarization on light-evoked EPSCs was strongly reduced in the presence of 10 mM BAPTA. The degree of EPSC inhibition by the prepulse holding potential followed the current-voltage relationship of the Ca2+ current found in the ganglion cell. In the presence of the NMDA receptor antagonist AP-7, glutamate-dependent current was nearly abolished when high Ca2+ was substituted for high Na+ solution. The release of Ca2+ from internal stores by caffeine or inositol trisphosphate reduced the EPSCs by 36 +/- 5 and 38 +/- 11 %, respectively, and abolished the inhibitory effect of depolarization. The inhibitory effect of depolarization on EPSCs was reduced 5-fold in the presence of AP-7, but was not reduced by the AMPA receptor antagonist CNQX. Neither inhibition of Ca2+-calmodulin-dependent enzymes, nor inhibition of protein kinase A or C had any significant effect on the depolarization-induced inhibition of EPSCs. Our data suggest that elevation of [Ca2+]i, through voltage-gated channels or by release from intracellular stores, reduced primarily the NMDA component of the light-evoked EPSCs.
机译：全细胞膜片钳技术用于研究sal内视网膜神经节细胞的开关神经节细胞内Ca2 +对光诱发的EPSC的影响。 AMPA和NMDA受体均对光诱发的反应有贡献。在存在士的宁和微小毒素的情况下，神经节细胞对光的发生和响应具有-70 mV的瞬时内向电流。当在光刺激之前进行从-70到0 mV的去极化步骤时，这些电流降低了35 +/- 3％。在10 mM BAPTA存在下，去极化对光诱发的EPSC的抑制作用大大降低。前脉冲保持电位对EPSC的抑制程度遵循神经节细胞中Ca2 +电流的电流-电压关系。在NMDA受体拮抗剂AP-7的存在下，当用高Ca2 +代替高Na +溶液时，谷氨酸依赖性电流几乎消失。咖啡因或肌醇三磷酸从内部储存区释放Ca2 +可使EPSC分别降低36 +/- 5和38 +/- 11％，并消除了去极化的抑制作用。在AP-7存在下，去极化对EPSC的抑制作用降低了5倍，但AMPA受体拮抗剂CNQX并未降低。抑制Ca2 +-钙调蛋白依赖性酶，或抑制蛋白激酶A或C对去极化诱导的EPSC抑制均无明显影响。我们的数据表明，通过电压门控通道或通过从细胞内存储释放，[Ca2 +] i的升高主要降低了光诱发的EPSC的NMDA成分。

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