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[目的]通过观察小鼠脑部电位和神经递质的变化,初步探讨其引发小鼠成瘾性及毒性的机制。[方法]造模后进行小鼠脑区定位,记录小鼠被动吸烟后脑区电位的变化并观察脑区神经递质的变化。[结果]1.诱发电位:(1)嗅球部诱发电位与自发电位比较:ETS刺激时,波形变化显著。(2)伏隔核部位诱发电位与自发电位比较:Nic刺激时,波形变化显著。(3)Nic刺激时,小鼠黑质部位诱发电位与自发电位比较,波形变化显著;ETS刺激时,小鼠黑质部位诱发电位与自发电位比较,波形变化显著。2.免疫组织化学结果:(1)GABA在小鼠大脑皮层、海马部位的表达,ETS暴露组阳性细胞数量明显减少(P﹤0.05)。(2)nAChR在大脑皮层的表达,ETS吸入组阳性表达明显增加(P﹤0.05)。(3)NMDAR在小鼠大脑皮层、纹状体皮质的表达,ETS吸入组、Nic吸入组阳性表达增加明显(P﹤0.05)。[结论]ETS、Nic可诱发小鼠嗅球、伏隔核、黑质等部位产生特征性OERP及导致大脑皮层、下丘脑等部位神经递质及受体表达的变化。
[Objective] To investigate the mechanism of mouse addiction and toxicity by observing the changes of brain electric potential and neurotransmitter in mice. [Method] After modeling, the brain regions of mice were located and the changes of brain potentials after passive smoking were recorded and the changes of neurotransmitters in brain regions were observed. [Results] 1. Evoked potentials: (1) Comparison of evoked potentials and spontaneous potentials in olfactory bulb: The waveform changes significantly when stimulated by ETS. (2) Evoked potentials compared with spontaneous potentials in nucleus accumbens: The waveform changes significantly when Nic stimulates. (3) Compared with spontaneous potentials, the evoked potentials of substantia nigra in mice were significantly increased when Nic stimulated. The evoked potentials of substantia nigra of ETS were significantly different from those of spontaneous potentials. Immunohistochemical results: (1) The expression of GABA in mouse cerebral cortex and hippocampus significantly decreased the number of positive cells in ETS exposure group (P <0.05). (2) The expression of nAChR in the cerebral cortex, ETS inhalation group was significantly increased (P <0.05). (3) The positive expression of NMDAR in mouse cerebral cortex and striatum cortex, ETS inhalation group and Nic inhalation group increased significantly (P <0.05). [Conclusion] ETS and Nic can induce characteristic OERP in the olfactory bulb, nucleus accumbens, substantia nigra and other parts of the mice and result in changes of neurotransmitter and receptor expression in cerebral cortex and hypothalamus.