McBean D E, Sharkey J, Ritchie I M, Kelly P A
Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, U.K.
Neuroscience. 1990;38(1):271-5. doi: 10.1016/0306-4522(90)90391-g.
The amphetamine derivative methylenedioxyamphetamine selectively destroys serotoninergic terminals in the brain. We have studied the effects of this toxin upon resting cerebral function, as reflected in rates of glucose utilization. Rats were injected subcutaneously with either 1 ml/kg saline (n = 5) or 20 mg/kg methylenedioxyamphetamine (n = 5) twice daily for four days. Local cerebral glucose utilization was measured between six and nine weeks after treatment using [14C]2-deoxyglucose quantitative autoradiography. Samples of frontal cortex taken from these animals for in vitro [3H]paroxetine binding showed a 64% reduction in 5-hydroxytryptamine uptake sites. In the majority of the 31 functionally diverse brain areas analysed, no significant changes were measured, but significant (P less than 0.05) increases in glucose use were found in neocortical regions e.g. anterior cingulate cortex (+16%) and sensorimotor cortex (+21%). However, the most profound increases were found in globus pallidus (+30%) and hippocampus molecular layer (+34%). It would appear, therefore, that treatment with methylenedioxyamphetamine results in long-lasting alterations in cerebral functional activity.
苯丙胺衍生物亚甲二氧基苯丙胺可选择性破坏大脑中的5-羟色胺能终末。我们研究了这种毒素对静息脑功能的影响，这可通过葡萄糖利用率来反映。大鼠每天皮下注射1次，每次1 ml/kg生理盐水（n = 5）或20 mg/kg亚甲二氧基苯丙胺（n = 5），共注射4天。在治疗后6至9周，使用[14C]2-脱氧葡萄糖定量放射自显影法测量局部脑葡萄糖利用率。从这些动物身上获取额叶皮质样本进行体外[3H]帕罗西汀结合试验，结果显示5-羟色胺摄取位点减少了64%。在所分析的31个功能各异的脑区中，大多数区域未检测到显著变化，但在新皮质区域，如前扣带回皮质（增加16%）和感觉运动皮质（增加21%），发现葡萄糖利用率有显著（P<0.05）增加。然而，苍白球（增加30%）和海马分子层（增加34%）的葡萄糖利用率增加最为显著。因此，看来用亚甲二氧基苯丙胺治疗会导致脑功能活动的长期改变。
