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慢性使用 crack cocaine 引起的行为和神经生物学改变。

Behavioral and neurobiological alterations induced by chronic use of crack cocaine.

机构信息

Departamento de Biociências, Universidade Federal de São Paulo (UNIFESP), Rua Silva Jardim, 136, 11015-20 Santos SP, Brazil.

Departamento de Biociências, Universidade Federal de São Paulo (UNIFESP), Rua Silva Jardim, 136, 11015-20 Santos SP, Brazil, e-mail:

出版信息

Rev Neurosci. 2019 Dec 18;31(1):59-75. doi: 10.1515/revneuro-2018-0118.

Abstract

Crack cocaine is the crystal form of cocaine and can be smoked, and rapidly absorbed, and, in part for this reason, is potently addictive. It is hypothesized that crack cocaine is able to induce important changes in different tissues and organs, and thus dramatically alter behavior. Nevertheless, which alterations in the central nervous system are related to its frequent use is still a matter of discussion. The present study is a literature review of articles published between the years 2008 and 2018 on the theme 'crack cocaine and brain' available in PUBMED, MEDLINE, EMBASE, and Google scholar databases. The results show that the use of crack cocaine induces important behavioral, neuroanatomical, and biochemical alterations. The main behavioral sequelae include cognitive and emotional changes, such as increased anxiety and depressive symptoms, attention and memory deficits, and hyperactivity. Among the neurobiological alterations are reductions in the activity of the prefrontal, anterior cingulate cortex, and nucleus accumbens. Molecular changes include decreases in neurotrophic factors and increases in oxidative stress and inflammatory cytokines, which may be responsible for the morphological alterations observed. It is also hypothesized that these neurobiological changes might explain the emotional and cognitive dysfunctions experienced by crack cocaine addicts.

摘要

快克可卡因是可卡因的晶体形式,可以被吸食,且能迅速被吸收,部分由于这个原因,它具有很强的成瘾性。据推测,快克可卡因能够诱导不同组织和器官的重要变化,从而显著改变行为。然而,其频繁使用与中枢神经系统的哪些改变有关,仍然是一个讨论的话题。本研究是对 2008 年至 2018 年间在 PUBMED、MEDLINE、EMBASE 和谷歌学术数据库中发表的关于“快克可卡因和大脑”主题的文章进行的文献回顾。结果表明,使用快克可卡因会引起重要的行为、神经解剖和生化改变。主要的行为后遗症包括认知和情绪变化,如焦虑和抑郁症状增加、注意力和记忆缺陷以及多动。神经生物学改变包括前额叶、前扣带回皮质和伏隔核活动减少。分子变化包括神经营养因子减少和氧化应激及炎性细胞因子增加,这可能是观察到的形态改变的原因。还有假设认为,这些神经生物学变化可能解释了快克可卡因成瘾者经历的情绪和认知功能障碍。

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