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首页> 外文期刊>The European Journal of Neuroscience >Persistent cerebrovascular effects of MDMA and acute responses to the drug.
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Persistent cerebrovascular effects of MDMA and acute responses to the drug.

机译：MDMA的持久性脑血管作用和对该药物的急性反应。

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摘要

Acutely, 3,4,-methylenedioxymethamphetamine (MDMA) induces cerebrovascular dysfunction [Quate et al., (2004)Psychopharmacol., 173, 287-295]. In the longer term the same single dose results in depletion of 5-hydroxytrptamine (5-HT) nerve terminals. In this study we examined the cerebrovascular consequences of this persistent neurodegeneration, and the acute effects of subsequent MDMA exposure, upon the relationship that normally exists between local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCMRglu). Dark agouti (DA) rats were pre-treated with 15 mg/kg i.p. MDMA or saline. Three weeks later, rats from each pre-treatment group were treated with an acute dose of MDMA (15 mg/kg i.p.) or saline. Quantitative autoradiographic imaging was used to measure LCBF or LCMRglu with [(14)C]-iodoantipyrine and [(14)C]-2-deoxyglucose, respectively. Serotonergic terminal depletion was assessed using radioligand binding with [(3)H]-paroxetine and immunohistochemistry. Three weeks after MDMA pre-treatment there were significant reductions in densities of 5-HT transporter (SERT)-positive fibres (-46%) and [(3)H]-paroxetine binding (-47%). In animals pre-treated with MDMA there were widespread significant decreases in LCMRglu, but no change in LCBF indicating a persistent loss of cerebrovascular constrictor tone. In both pre-treatment groups, acute MDMA produced significant increases in LCMRglu, while LCBF was significantly decreased. In 50% of MDMA-pre-treated rats, random areas of focal hyperaemia indicated a loss of autoregulatory capacity in response to MDMA-induced hypertension. These results suggest that cerebrovascular regulatory dysfunction resulting from acute exposure to MDMA is not diminished by previous exposure, despite a significant depletion in 5-HT terminals. However, there may be a sub-population, or individual circumstances, in which this dysfunction develops into a condition that might predispose to stroke.
机译：急性地，3，4，-亚甲二氧基甲基苯丙胺（MDMA）诱导脑血管功能障碍[Quate等人，（2004）Psychopharmacol。，173，287-295]。从长远来看，相同的单剂量可导致5-羟色胺（5-HT）神经末梢消耗。在这项研究中，我们检查了这种持续性神经变性的脑血管后果，以及随后的MDMA暴露对局部脑血流量（LCBF）和局部脑葡萄糖利用（LCMRglu）之间通常存在的关系的急性影响。用15 mg / kg i.p.预处理暗粉刺（DA）大鼠。摇头丸或盐水。三周后，用急性剂量的MDMA（15mg / kg i.p.）或盐水治疗来自每个预处理组的大鼠。定量放射自显影成像分别用于测量[[14] C]-碘安替比林和[[14] C] -2-脱氧葡萄糖的LCBF或LCMRglu。使用[[3] H]-帕罗西汀与放射配体结合和免疫组织化学评估血清素能终末消耗。 MDMA预处理三周后，5-HT转运蛋白（SERT）阳性纤维的密度（-46％）和[（3H）]-帕罗西汀结合（-47％）明显降低。在用MDMA预处理的动物中，LCMRglu普遍存在明显下降，但LCBF没有变化，表明脑血管收缩张力持续下降。在两个预处理组中，急性MDMA均导致LCMRglu显着增加，而LCBF则显着下降。在50％的MDMA预处理大鼠中，随机区域的局灶性充血表明对MDMA诱发的高血压有反应，其自动调节能力下降。这些结果表明，尽管5-HT末端明显耗竭，但急性暴露于MDMA并不会减轻因急性暴露于MDMA而引起的脑血管调节功能障碍。但是，可能存在某些人群或个别情况，其中该功能障碍会发展为容易中风的状况。

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