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目的阐明伤害性电刺激隐神经(saphenous nerve,SN)能否引起扣带回前部(anterior cingulategyrus,ACG)神经元c-Fos基因表达及其发生机制。方法用免疫组化方法研究伤害性电刺激SN后不同时间,ACG神经元c-Fos基因表达的变化,以及尾静脉注射α-氨基3-羟基5-甲基4-异恶唑丙酸/海人藻氨酸(α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid/kainate,AMPA/kainate)受体拮抗剂受体是谷氨酸受体之一,6-氰基-7-硝基喹喔啉-2,3-二酮(6-cyano-7-nitroquinoxaline-2,3-dike-tone,CNQX)对该变化的影响。结果伤害性电刺激SN后30 min ACG神经元Fos蛋白表达明显增加,60 min增加最明显,120 min后开始消退;并且尾静脉注射CNQX拮抗了伤害性电刺激SN引起的ACG神经元Fos蛋白表达的显著增加。结论伤害性电刺激SN能够引起ACG神经元Fos蛋白表达的显著增加,这种表达呈时间依赖性,提示ACG存有SN代表区,能够感受SN传入的伤害性信息;CNQX拮抗了伤害性电刺激SN引起的ACG神经元Fos蛋白表达的显著增加,提示AMPA/kainate受体参与此过程。
Objective To investigate whether noxious electrical stimulation of saphenous nerve (SN) can induce c-Fos gene expression and its mechanism in anterior cingulate gyrus (ACG) neurons. Methods The expression of c-Fos gene in ACG neurons was detected by immunohistochemistry at different time points after noxious electrical stimulation. The effects of α-amino 3-hydroxy 5-methyl 4-isoxazole propionate One of the receptors for glutamate receptors is the receptor for alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (kainate) The effect of 6-cyano-7-nitroquinoxaline-2,3-dike-tone (CNQX) on this change was investigated. Results The expression of Fos protein in ACG neurons was significantly increased 30 min after noxious stimulation, and the most obvious increase was observed at 60 min after 60 niggests SN, and began to subside after 120 min; and CNQX was injected into caudal vein to antagonize the expression of Fos protein in ACG neurons induced by noxious stimulation A significant increase. Conclusions The nociceptive electrical stimulation of SN can induce a significant increase of Fos protein expression in ACG neurons, which is time-dependent. It suggests that ACG contains the SN representative region and can infect SN with the nociceptive information. CNQX antagonizes nociception Stimulation of SN induced ACG neurons Fos protein expression was significantly increased, suggesting that AMPA / kainate receptors involved in this process.