When PRG-1 was restored to individual neurons, activity levels returned to normal.
当PRG - 1贮存于单个神经元时，兴奋水平回归正常。
Animals lacking both PRG-1 and the LPA receptor didn't have epilepsy either, more evidence that PRG-1 ACTS via the lipid signal.
当动物缺乏PRG - 1基因和溶血磷酯酸受体时，也不会发生癫痫，更多证据说明prg - 1基因是通过磷脂信号起作用的。
The team led by Robert Nitsch of Universitätsmedizin Berlin speculates that changes in lipid phosphate signaling and PRG-1 function may be unrecognized causes of epilepsy.
由柏林医科大学的Robert Nitsch带领的团队推测磷酸酯信号和PRG-1功能的改变可能是癫痫未发现的原因。
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