【摘要】 目的研究尾核中一氧化氮在痛觉调制中的作用机制。方法大鼠尾核内微量注射L-精氨酸、Nω-硝基-L-精氨酸甲酯、生理盐水,应用逆转录-聚合酶链反应测定4,8,12,24和48 h大鼠尾核nNOS mRNA表达的变化;新生Wistar大鼠尾核神经元原代培养液中加入L-精氨酸、Nω-硝基-L-精氨酸甲酯、生理盐水,观察给药12 h尾核nNOS mRNA表达的变化。结果大鼠尾核给药24 h内L-精氨酸组nNOS mRNA表达较正常增强(P<0.05),而Nω-硝基-L-精氨酸甲酯组nNOS mRNA表达较正常减弱(P<0.05),48 h恢复正常。体外尾核原代神经元培养,nNOS mRNA表达的变化趋势和在体实验相一致。结论中枢神经系统尤其是尾核中NOS活性是一氧化氮作为神经递质或调质参与中枢痛觉调制的关键因素之一。更多还原

【Abstract】 Objective To observe the modulation of nitric oxide(NO) on pain threshold(PT) in the caudate nucleus.Methods Microdose of L-arginine(L-Arg),N(omega)-nitro-L-arginine methyl ester(L-NAME) or normal sodium(NS) was injected into rat caudate nucleus.The expression of caudate nucleus nNOS mRNA were detcted by reverse transcription-poly-merase chain reaction(RT-PCR) at 4,8,12,24 and 48 hours after administration.The primary neurons derived from caudate nucleus of neonatal rats were cultured in vitro.L-Arg,L-NAME and NS were seperately added into culture solution.The changes of cultured caudate nucleus nNOS mRNA at 12 hours after administration were examined by RT-PCR.Results The level of nNOS mRNA was significantly increased when L-Arg were administratled 12hours.(P﹤0.05),but which was significantly decreased when L-NAME were administrate 24 hours(P﹤0.05).Either the increased or decreased level of nNOS mRNA returned to normal at 48 hours of administration.The same result was found in the primary caudate nucleus neurons cultured in vitro.Conclusion NOS activity is one of the key factors of pain modulation induced by NO,a neurotransmitter or neuromodulator.更多还原