Diamond J S, Copenhagen D R
Bioengineering Graduate Group, University of California, San Francisco 94143-0730.
Neuron. 1993 Oct;11(4):725-38. doi: 10.1016/0896-6273(93)90082-3.
To examine how light-evoked excitatory synaptic inputs to retinal ganglion cells are transformed into output patterns of activity, action potentials were recorded with cell-attached patch-clamp techniques, and then EPSCs and EPSPs were recorded from the same cell in the whole-cell configuration. AP7, an NMDA antagonist, reduced the light-evoked peak spike frequency 36% +/- 21% (mean +/- SD) and reduced the EPSC amplitude, indicating a major role for NMDA receptors in the light response. CNQX, a non-NMDA receptor antagonist, reduced the light-evoked peak spike frequency 28% +/- 22%. CNQX also caused a voltage- and magnesium-dependent delay in spike onset. AP7 and CNQX, however, did not differ significantly in their effect on the EPSC time course, indicating that postsynaptic cellular properties are responsible for the delay observed in the presence of CNQX. These results show that the NMDA receptor contribution to the excitatory response is increased as the cell is depolarized from rest by non-NMDA input.
为了研究视网膜神经节细胞的光诱发兴奋性突触输入是如何转化为活动输出模式的，采用细胞贴附式膜片钳技术记录动作电位，然后在全细胞模式下从同一细胞记录兴奋性突触后电流（EPSC）和兴奋性突触后电位（EPSP）。NMDA拮抗剂AP7使光诱发的峰值放电频率降低了36%±21%（平均值±标准差），并降低了EPSC幅度，表明NMDA受体在光反应中起主要作用。非NMDA受体拮抗剂CNQX使光诱发的峰值放电频率降低了28%±22%。CNQX还导致了放电起始的电压和镁依赖性延迟。然而，AP7和CNQX对EPSC时间进程的影响没有显著差异，表明突触后细胞特性是CNQX存在时观察到的延迟的原因。这些结果表明，随着细胞因非NMDA输入而从静息状态去极化，NMDA受体对兴奋性反应的贡献增加。
