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目的观察子宫内海洛因暴露对小鼠前额叶皮层(PFC)、海马(HP)和伏核(Acb)脑区磷酸化ERK1/2(p-ERK1/2)表达的影响,探讨ERK MAPK细胞信号转导通路是否参与了发育期海洛因暴露导致小鼠神经行为缺陷的分子机制。方法于胚胎鼠9~18日龄时,每天给孕鼠皮下注射海洛因10 mg/kg一次,建立宫内海洛因暴露小鼠模型。按出生前处理将小鼠分为海洛因组(Her)和盐水组(Sal)。RT-PCR和蛋白免疫印迹法检测两组小鼠前PFC,HP和Acb三个脑区组织p-ERK1/2的表达变化。结果与Sal组相比,Her组小鼠的体重无明显变化;p-ERK1/2的mRNA和蛋白表达在三个脑区无明显改变。结论发育期10 mg/kg海洛因暴露未损伤小鼠的体格发育,海洛因可能通过ERK1/2 MAPK信号通路以外的机制导致神经行为缺陷。
Objective To investigate the effect of intrauterine heroin exposure on the expression of phosphorylated ERK1 / 2 (p-ERK1 / 2) in mouse prefrontal cortex (PFC), hippocampus (HP) and nucleus accumbens (Acb) Whether the conduction pathway participates in the molecular mechanism of neurobehavioral defects in mice during developmental heroin exposure. Methods The pregnant rats were subcutaneously injected with heroin 10 mg / kg once daily for 9-18 days to establish intrauterine heroin exposure model in mice. The mice were divided into heroin group and saline group according to prenatal treatment. RT-PCR and Western blotting were used to detect the expression of p-ERK1 / 2 in the three brain regions before PFC, HP and Acb. Results Compared with Sal group, there was no significant change in body weight in Her group. The expression of p-ERK1 / 2 mRNA and protein did not change in all three brain regions. Conclusions Physiological development is not observed in heroin-exposed mice exposed to 10 mg / kg heroin at the developmental stage. Heroin may cause neurobehavioral deficits through mechanisms other than ERK1 / 2 MAPK signaling.