Marie Curie Chairs Program, Department of Pharmacology and Physiology of Nervous System, Institute of Psychiatry and Neurology, 02-957, Warsaw, Poland.
Neurochem Res. 2012 Feb;37(2):436-47. doi: 10.1007/s11064-011-0630-z. Epub 2011 Oct 21.
Thimerosal, a mercury-containing vaccine preservative, is a suspected factor in the etiology of neurodevelopmental disorders. We previously showed that its administration to infant rats causes behavioral, neurochemical and neuropathological abnormalities similar to those present in autism. Here we examined, using microdialysis, the effect of thimerosal on extracellular levels of neuroactive amino acids in the rat prefrontal cortex (PFC). Thimerosal administration (4 injections, i.m., 240 μg Hg/kg on postnatal days 7, 9, 11, 15) induced lasting changes in amino acid overflow: an increase of glutamate and aspartate accompanied by a decrease of glycine and alanine; measured 10-14 weeks after the injections. Four injections of thimerosal at a dose of 12.5 μg Hg/kg did not alter glutamate and aspartate concentrations at microdialysis time (but based on thimerosal pharmacokinetics, could have been effective soon after its injection). Application of thimerosal to the PFC in perfusion fluid evoked a rapid increase of glutamate overflow. Coadministration of the neurosteroid, dehydroepiandrosterone sulfate (DHEAS; 80 mg/kg; i.p.) prevented the thimerosal effect on glutamate and aspartate; the steroid alone had no influence on these amino acids. Coapplication of DHEAS with thimerosal in perfusion fluid also blocked the acute action of thimerosal on glutamate. In contrast, DHEAS alone reduced overflow of glycine and alanine, somewhat potentiating the thimerosal effect on these amino acids. Since excessive accumulation of extracellular glutamate is linked with excitotoxicity, our data imply that neonatal exposure to thimerosal-containing vaccines might induce excitotoxic brain injuries, leading to neurodevelopmental disorders. DHEAS may partially protect against mercurials-induced neurotoxicity.
硫柳汞,一种含汞的疫苗防腐剂,被怀疑是神经发育障碍病因学中的一个因素。我们之前的研究表明,它对婴儿大鼠的给药会导致行为、神经化学和神经病理学异常,类似于自闭症中存在的异常。在这里,我们使用微透析检查了硫柳汞对大鼠前额叶皮质(PFC)细胞外神经活性氨基酸水平的影响。硫柳汞给药(4 次肌肉注射,出生后第 7、9、11、15 天,240μgHg/kg)引起氨基酸溢出的持久变化:谷氨酸和天冬氨酸增加,同时甘氨酸和丙氨酸减少;在注射后 10-14 周测量。4 次 12.5μgHg/kg 剂量的硫柳汞注射不会改变微透析时的谷氨酸和天冬氨酸浓度(但根据硫柳汞药代动力学,可能在其注射后很快就有效)。将硫柳汞应用于 PFC 灌流液中会迅速增加谷氨酸溢出。同时给予神经甾体脱氢表雄酮硫酸盐(DHEAS;80mg/kg;腹腔内)可防止硫柳汞对谷氨酸和天冬氨酸的作用;类固醇本身对这些氨基酸没有影响。DHEAS 与硫柳汞在灌流液中的共同应用也阻断了硫柳汞对谷氨酸的急性作用。相比之下,DHEAS 本身减少了甘氨酸和丙氨酸的溢出,略微增强了硫柳汞对这些氨基酸的作用。由于细胞外谷氨酸的过度积累与兴奋性毒性有关,我们的数据表明,新生儿接触含硫柳汞的疫苗可能会导致兴奋性毒性脑损伤,从而导致神经发育障碍。DHEAS 可能部分保护免受汞剂诱导的神经毒性。