Okazaki Yuka, Morimoto Takeshi, Sawai Hajime
Department of Physiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Neurosci Res. 2008 Jun;61(2):129-35. doi: 10.1016/j.neures.2008.01.016. Epub 2008 Feb 6.
We previously showed the enhancement of survival of retinal ganglion cells (RGCs) by electrical stimulation (ES) of the optic nerve (ON) stump in adult rats. To elucidate the mechanisms underlying the survival enhancement, we determined whether the neuroprotective effect of ES is affected by the following parameters: stimulation time, frequency of current pulses and starting of ES. ES for 10min immediately after ON transection was not effective in increasing the number of surviving RGCs 7 days after the transection, but that for 30min was effective. ES at 20Hz was the most effective, when applied just after axotomy. When the starting of ES to the ON was shifted either 3h after or 4h before the axotomy, the neuroprotective effect of ES was not observed. These results suggest that the electrical activation of RGCs and/or the transected ON interfere with early events after axotomy that leads to RGC death.
我们之前发现，对成年大鼠的视神经残端进行电刺激（ES）可提高视网膜神经节细胞（RGCs）的存活率。为了阐明存活率提高背后的机制，我们确定了ES的神经保护作用是否受以下参数影响：刺激时间、电流脉冲频率以及ES开始的时间。视神经横断后立即进行10分钟的ES对提高横断7天后存活的RGCs数量无效，但30分钟的ES则有效。轴突切断后立即施加ES时，20Hz的刺激最为有效。当ES对视神经的施加时间在轴突切断后3小时或前4小时改变时，未观察到ES的神经保护作用。这些结果表明，RGCs和/或横断的视神经的电激活会干扰轴突切断后导致RGC死亡的早期事件。
