中文摘要：

目的：观察瘦素对幼龄厌食大鼠下丘脑腹内侧核（VMN）神经元膜电位的影响。方法：利用红外可视膜片钳技术记录对照组、模型组两组动物VMN神经元的膜电位，分析瘦素对VMN神经元膜电位的影响。结果：瘦素使两组动物大部分神经元去极化，组间比较无显著性差异。少数VMN神经元在瘦素作用下超极化，组间比较亦无显著性差异。然而，模型组VMN神经元的膜电位被瘦素去极化而导致自发放电增加的细胞比例增多，被瘦素超极化而自发放电减少的细胞比例减少，对瘦素无反应的细胞比例也减少。结论：造模因素可能通过提高VMN对瘦素的整体敏感性，使VMN发出过度的饱信号，从而产生厌食，这应当是小儿厌食发生发展的中枢机制之一。

英文摘要：

Objective ： To study the effects of Leptin adjusting membrane potential of VMN neurons in juvenile anorexia rats. Methods： By using infrared-visualized patch-clamp technique, we recorded the membrane potential of two groups which were the control group and model group, and analyzed the effects of Leptin on the membrane potential of VMN neurons. Results ： Leptin depolarized the most neurons of the two groups and hyperpolarized the minor neurons, but there had no significant difference between the two groups. However, Leptin increased the proportion of the spontaneous discharge neurons with depolarizing membrane potential of the VMN neurons in model group, but decreased the proportion with hyperpolarizing membrane potential of the VMN neurons. The neurons had no response to Leptin were reducted in model group. Conclusion： Model group can raise up the sensitivity of VMN neurons to LEP and result in anorexia, and sent out excessive satisfied signal to product anorexia. This should be one of the center mechanism about the juvenile anorexia development.