The effect of testosterone upon methamphetamine neurotoxicity of the nigrostriatal dopaminergic system
The effect of testosterone upon methamphetamine neurotoxicity of the nigrostriatal dopaminergic system
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DOI：
10.1016/s0006-8993(00)03221-2
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发表时间：
2001-02-16
期刊：
影响因子：
2.9
通讯作者：
Dluzen, DE
中科院分区：
文献类型：
--
作者：
Gao, XM;Dluzen, DE
性腺类固醇激素雌激素（E）可以作为黑质纹状体多巴胺能（NSDA）神经毒性的神经保护剂，然而，关于睾酮（T）在这种能力中的作用的信息非常有限。在本报告中，在性腺切除的雌性和雄性 CD-1 小鼠中检查了 T 对甲基苯丙胺 (MA) 诱导的 NSDA 系统神经毒性的影响。在实验 I 中，接受 T 治疗的卵巢切除小鼠的纹状体多巴胺 (DA) 浓度和输出量与 MA 后未接受 T 治疗的小鼠没有显着差异。这些结果表明，在卵巢切除的 CD-1 小鼠中，T 不能作为 MA 诱导的 NSDA 神经毒性的调节剂。在实验2中，MA后T处理、未T处理以及E处理的睾丸切除小鼠的DA浓度或输出没有显着差异。实验2的结果表明，在去卵巢小鼠中报告的E的神经保护作用在雄性小鼠中没有观察到。在雄性小鼠中，T 似乎也没有起到 MA 神经毒性调节剂的作用。 T和E对MA诱导的NSDA系统神经毒性的这些影响对于在NSDA神经毒性动物模型和帕金森病中观察到的性别差异具有重要意义。 (C) 2001 Elsevier Science B.V. 保留所有权利。
The gonadal steroid hormone estrogen (E) can function as a neuroprotectant of nigrostriatal dopaminergic (NSDA) neurotoxicity, however, there exists very limited information on the role of testosterone (T) in this capacity. In the present report, the effects of T on methamphetamine (MA) induced neurotoxicity of the NSDA system were examined in gonadectomized female and male CD-1 mice. In Experiment I, striatal dopamine (DA) concentrations and output from T-treated ovariectomized mice were not significantly different from that of non-T-treated mice following MA. These results suggest that T is not functioning as a modulator of MA-induced NSDA neurotoxicity in ovariectomized CD-1 mice. In Experiment 2, there were no significant differences in DA concentrations or output among T-treated, non-T-treated as well as E-treated orchidectomized mice following MA. The results of Experiment 2 indicate that the neuroprotective effect of E reported within ovariectomized mice is not seen in male mice. Nor does T appear to function as a modulator of MA neurotoxicity in male mice. These effects of T and E upon the MA induced neurotoxicity of the NSDA system have important implications for the gender differences which are observed in animal models of NSDA neurotoxicity and in Parkinson's disease. (C) 2001 Elsevier Science B.V. All rights reserved.