Neural degeneration following chronic stimulant abuse reveals a weak link in brain, fasciculus retroflexus, implying the loss of forebrain control circuitry
Neural degeneration following chronic stimulant abuse reveals a weak link in brain, fasciculus retroflexus, implying the loss of forebrain control circuitry
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DOI：
10.1016/s0924-977x(02)00020-2
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发表时间：
2002-08-01
影响因子：
5.6
通讯作者：
Ellison, G
中科院分区：
文献类型：
--
作者：
Ellison, G
越来越多的证据表明，在持续给药或滥用药物后，反曲束（FR）是一个“薄弱环节”。各种主要增强多巴胺的药物，包括D-苯丙胺、甲基苯丙胺、MDMA、可卡因和卡西酮，都诱导从外侧缰通过FR鞘到中脑细胞如SN、VTA和中缝的轴突变性。对于某些药物，如可卡因，这实际上是大脑中诱导的唯一变性。连续尼古丁也选择性地诱导FR的变性，但在另一半的束，即在从内侧缰通过束的核心到脚间核的轴突。这条遗传学上原始的神经束将前脑的大部分负反馈带回中脑的奖赏细胞，而这些下行控制通路在模拟药物狂欢后受到损害的发现，不仅对药物成瘾理论有影响，而且对一般精神病也有影响。(C)2002 Elsevier Science B. V.保留所有权利。
There is increasing evidence that the fasciculus retroflexus (FR) represents a 'weak link' following the continuous administration of drugs, of abuse. A variety of drugs which predominantly potentiate dopamine, including D-amphetamine, methamphetamine, MDMA, cocaine, and cathinone, all induce degeneration in axons from lateral habenula, through the sheath of FR, to midbrain cells such as SN, VTA, and raphe. For some drugs, such as cocaine, this is virtually the only degeneration induced in brain. Continuous nicotine also selectively induces degeneration in FR, but in the other half of the tract, i.e. in axons from medial habenula through the core of the tract to inter-peduncular nucleus. This phylogenetically primitive tract carries much of the negative feedback from forebrain back onto midbrain reward cells, and the Finding that these descending control pathways are compromised following simulated drug binges has implications for theories of drug addiction but also psychosis in general. (C) 2002 Elsevier Science B.V. All rights reserved.