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1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)而非甲基苯丙胺诱导的帕金森症会扩展至肠道中的儿茶酚胺能神经元。

MPTP- but not methamphetamine-induced parkinsonism extends to catecholamine neurons in the gut.

作者信息

Natale Gianfranco, Kastsiuchenka Olga, Pasquali Livia, Ruggieri Stefano, Paparelli Antonio, Fornai Francesco

机构信息

Department of Human Morphology and Applied Biology, University of Pisa, Pisa, Italy.

出版信息

Ann N Y Acad Sci. 2008 Oct;1139:345-9. doi: 10.1196/annals.1432.015.

Abstract

Methamphetamine (METH) produces nigrostriatal dopamine (DA) loss, partly resembling that which occurs in Parkinson's disease (PD). In PD there is also a marked alteration in the gut. Given the similarities between the central DA denervation produced by METH and PD, in the present study we evaluated the alterations in the gut following upon METH administration. To compare these effects with those occurring in PD, we also administered the parkinsonism-inducing neurotoxin MPTP. METH and MPTP were administered to mice, and after 7 days we investigated the immunostaining for tyrosine hydroxylase in nervous plexuses. These data indicate that METH did not alter the catecholamine-containing axons and autonomic neurons, while MPTP markedly reduced these components.

摘要

甲基苯丙胺(METH)会导致黑质纹状体多巴胺(DA)丧失,部分类似于帕金森病(PD)中出现的情况。在帕金森病中,肠道也有明显改变。鉴于METH导致的中枢DA去神经支配与帕金森病之间的相似性,在本研究中,我们评估了给予METH后肠道的改变。为了将这些效应与帕金森病中的效应进行比较,我们还给予了诱发帕金森症的神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)。将METH和MPTP给予小鼠,7天后,我们研究了神经丛中酪氨酸羟化酶的免疫染色。这些数据表明,METH并未改变含儿茶酚胺的轴突和自主神经元,而MPTP则显著减少了这些成分。

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