短波胃电刺激对大鼠孤束核及下丘脑c—fos表达的影响及其机制

Effect of short pulse gastric electrical stimulation on the c-los expression in nucleus tractus solitarius and hypothalamus and its possible mechanism

目的探讨肠肌间神经丛及中枢神经系统相关核团（孤束核及下丘脑）是否参与介导外源性短波胃电刺激调控中枢感觉功能。方法雄性Wistar大鼠15只，分为对照组、胃电刺激组、去肠肌间神经丛组，均于胃底、胃体交界处植入一对电极，去肠肌间神经丛组大鼠同时胃浆膜面予苯扎氯胺处理，后两组均予短波胃电刺激，持续30min。SP免疫组化法观察延髓孤束核及下丘脑c-los表达。结果胃电刺激组和去肠肌间神经丛组大鼠每高倍视野下孤束核处c-los阳性神经元数量分别为（71．6±7．4）和（63．4±10．8）个，下丘脑处则分别为（224．2±47．3）和（249．1±44．0）个，两组间差异无统计学意义（P〉0．05），但均显著高于对照组[（36．4±8．6）和（90．2±47．3）个，P值均〈0．05]。结论孤束核及下丘脑可能是介导短波胃电刺激治疗作用的中枢核团，而肠神经系统不参与介导此作用。

Objective To investigate whether enteric nervous system（ENS） involve in mediating the effect of short pulse gastric electrical stimulation on c-fos expression in nucleus tractus solitarius （NTS） and hypothalamus. Methods Fifteen Wistar rats were divided into control group, gastric electrical stimulation （GES） group and ENS free group with 5 rats each. A pair of electrodes was implanted on the gastric serosa. In ENS free group, 0.5% benzalkonii chloridum was applied on the serosa during the surgery. A set of short pulse GES with frequency of 20 cpm, pulse width of 300 us and amplitude of 2 mA was applied via the electrodes for 30 min in the stimulation group and ENS free group. The c-fos expression in NTS/hypothalamus was detected 1 h after the stimulation. Results The number of neuron with c-fos expression was （71.6±7.4）/HP in NTS group and （63.4±10.8）/ HP in ENS free group, both were significantly higher than those in control group （36.4±8.6/HP,P 〈0.05）. The number of neuron with c-fos expression in hypothalamus was higher in GES [（224.2±47.3）/HP] and ENS free groups [-（249.1±44.0）/HP] compared with control group[-（90.2±47.3）/ HP,P〈0.05]. There was no significant difference in c-fos expression in NTS/hypothalamus between GES group and ENS free group （P〉 0.05）. Conclusions Short pulse gastric electrical stimulation significantly increases c-fos expression in NTS/hypothalamus, which suggests that NTS/ hypothalamus may participate in mediating the effect of GES on gastric function. This effect may be not mediated by ENS.