Gorio A, Vergani L, Malosio M L, Lesma E, Di Giulio A M
Department of Medical Pharmacology, University of Milano, Italy.
Eur J Pharmacol. 1996 May 6;303(1-2):21-6. doi: 10.1016/0014-2999(96)00054-4.
The effects of neonatal 6-hydroxydopamine treatment on the brain of control rats and of rats perinatally exposed to morphine were examined. Noradrenaline levels were increased in the pons-medulla, mesencephalon and caudate of 8-week-old control rats lesioned with neonatal 6-hydroxydopamine; perinatal morphine treatment prevented such an increase. In the caudate, there was a loss of dopamine and an increase of serotonin following the neurotoxic lesion; exposure to perinatal morphine prevented the serotonin increase. Brain expression of synapsin I mRNA was particularly abundant in cerebral cortex, hippocampus, dentate gyrus and olfactory bulb. In perinatal morphine-treated rats, the expression of synapsin I mRNA was significantly reduced; interestingly, the neonatal treatment with 6-hydroxydopamine normalized its expression. Therefore, brain-reactive neurochemical changes triggered by 6-hydroxydopamine were suppressed by perinatal morphine exposure whereas the association of morphine exposure and 6-hydroxydopamine lesion promoted the normal mRNA expression of the synaptic marker synapsin I.
研究了新生期6-羟基多巴胺处理对对照大鼠以及围产期暴露于吗啡的大鼠大脑的影响。新生期用6-羟基多巴胺损伤的8周龄对照大鼠,其脑桥-延髓、中脑和尾状核中的去甲肾上腺素水平升高;围产期吗啡处理可阻止这种升高。在尾状核中,神经毒性损伤后多巴胺减少,血清素增加;围产期暴露于吗啡可阻止血清素增加。突触素I mRNA的脑表达在大脑皮层、海马、齿状回和嗅球中特别丰富。在围产期接受吗啡处理的大鼠中,突触素I mRNA的表达显著降低;有趣的是,新生期用6-羟基多巴胺处理可使其表达恢复正常。因此,围产期吗啡暴露抑制了由6-羟基多巴胺引发的脑反应性神经化学变化,而吗啡暴露与6-羟基多巴胺损伤的联合作用促进了突触标记物突触素I的正常mRNA表达。