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探索死后大脑中的杏仁核结构变化和信号通路：长期甲基苯丙胺成瘾的后果。

Exploring amygdala structural changes and signaling pathways in postmortem brains: consequences of long-term methamphetamine addiction.

作者信息

Azimzadeh Zahra, Omidvari Samareh, Niknazar Somayeh, Vafaei-Nezhad Saeed, Roozbahany Navid Ahmady, Abdollahifar Mohammad-Amin, Tahmasebinia Foozhan, Mahmoudiasl Gholam-Reza, Abbaszadeh Hojjat Allah, Darabi Shahram

机构信息

Hearing Disorders Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Laser Application in Medical Sciences Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Anat Cell Biol. 2024 Mar 31;57(1):70-84. doi: 10.5115/acb.23.193. Epub 2023 Nov 22.

DOI:10.5115/acb.23.193
PMID:37994041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10968194/
Abstract

Methamphetamine (METH) can potentially disrupt neurotransmitters activities in the central nervous system (CNS) and cause neurotoxicity through various pathways. These pathways include increased production of reactive nitrogen and oxygen species, hypothermia, and induction of mitochondrial apoptosis. In this study, we investigated the long-term effects of METH addiction on the structural changes in the amygdala of postmortem human brains and the involvement of the brain- cAMP response element-binding protein/brain-derived neurotrophic factor () and signaling pathways. We examined ten male postmortem brains, comparing control subjects with chronic METH users, using immunohistochemistry, real-time polymerase chain reaction (to measure levels of , and tumor necrosis factor-α []), Tunnel assay, stereology, and assays for reactive oxygen species (ROS), glutathione disulfide (GSSG), and glutathione peroxidase (GPX). The findings revealed that METH significantly reduced the expression of , and GPX while increasing the levels of GSSG, ROS, RIPK3, , and . Furthermore, METH-induced inflammation and neurodegeneration in the amygdala, with ROS production mediated by the and signaling pathways.

摘要

甲基苯丙胺（METH）可能会破坏中枢神经系统（CNS）中的神经递质活动，并通过各种途径导致神经毒性。这些途径包括活性氮和氧物种的产生增加、体温过低以及线粒体凋亡的诱导。在本研究中，我们调查了甲基苯丙胺成瘾对死后人类大脑杏仁核结构变化的长期影响，以及脑环磷酸腺苷反应元件结合蛋白/脑源性神经营养因子（）和信号通路的参与情况。我们检查了10个男性死后大脑，将对照受试者与慢性甲基苯丙胺使用者进行比较，采用免疫组织化学、实时聚合酶链反应（测量、和肿瘤坏死因子-α []的水平）、Tunnel检测、体视学以及活性氧（ROS）、谷胱甘肽二硫化物（GSSG）和谷胱甘肽过氧化物酶（GPX）检测。研究结果显示，甲基苯丙胺显著降低了、和GPX的表达，同时增加了GSSG、ROS、RIPK3、和的水平。此外，甲基苯丙胺诱导杏仁核中的炎症和神经退行性变，活性氧的产生由和信号通路介导。

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