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.

中文翻译：

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长期使用快克可卡因引起的行为和神经生物学改变

快克可卡因是可卡因的结晶形式，可以吸食并迅速吸收，部分原因是它具有很强的成瘾性。据推测，快克可卡因能够引起不同组织和器官的重要变化，从而显着改变行为。然而，中枢神经系统的哪些变化与其频繁使用有关，仍然是一个讨论问题。本研究是对 PUBMED、MEDLINE、EMBASE 和谷歌学术数据库中 2008 年至 2018 年间发表的主题为“快克可卡因和大脑”的文章的文献综述。结果表明，使用快克可卡因会引起重要的行为、神经解剖学和生化改变。主要的行为后遗症包括认知和情绪变化，例如焦虑和抑郁症状增加，注意力和记忆力减退，多动。神经生物学的改变包括前额叶、前扣带皮层和伏隔核的活动减少。分子变化包括神经营养因子的减少以及氧化应激和炎性细胞因子的增加，这可能是观察到的形态学改变的原因。还假设这些神经生物学变化可能解释可卡因成瘾者所经历的情绪和认知功能障碍。这可能是观察到的形态变化的原因。还假设这些神经生物学变化可能解释可卡因成瘾者所经历的情绪和认知功能障碍。这可能是观察到的形态变化的原因。还假设这些神经生物学变化可能解释可卡因成瘾者所经历的情绪和认知功能障碍。