Castilla-Ortega Estela, Ladrón de Guevara-Miranda David, Serrano Antonia, Pavón Francisco J, Suárez Juan, Rodríguez de Fonseca Fernando, Santín Luis J
Unidad de Gestión Clínica de Salud Mental, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Spain.
Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Instituto de Investigación Biomédica de Málaga (IBIMA), Facultad de Psicología, Universidad de Málaga, Spain.
Biochem Pharmacol. 2017 Oct 1;141:100-117. doi: 10.1016/j.bcp.2017.05.003. Epub 2017 May 6.
After discovering that addictive drugs alter adult neurogenesis, the potential role of adult-born hippocampal neurons in drug addiction has become a promising research field, in which cocaine is the most frequently investigated drug. Although a substantial amount of pre-clinical evidence has accumulated, additional studies are required to reveal the mechanisms by which cocaine modulates adult hippocampal neurogenesis (AHN) and determine whether these adult-born neurons have a role in cocaine-related behaviors, such as cocaine-mediated cognitive symptoms. First, this review will summarize the cocaine-induced alterations in a number of neurobiological factors (neurotransmitters, neurotrophins, glucocorticoids, inflammatory mediators) that likely regulate both hippocampal-dependent learning and adult hippocampal neurogenesis after cocaine exposure. A separate section will provide a detailed review of the available literature that challenges the common view that cocaine reduces adult hippocampal neurogenesis. In fact, cocaine has a short-term anti-proliferative role, but the young adult-born neurons are apparently spared, or even enhanced, following certain cocaine protocols. Thus, we will try to reconcile this evidence with the hippocampal-dependent cognitive symptoms that are typically observed in cocaine addicts, and we will propose new directions for future studies to test the relevant hypothesis. Based on the evidence presented here, the regulation of adult hippocampal neurogenesis might be one of the many mechanisms by which cocaine sculpts hippocampus-dependent learning.
在发现成瘾性药物会改变成体神经发生后,成年新生海马神经元在药物成瘾中的潜在作用已成为一个很有前景的研究领域,其中可卡因是研究最为频繁的药物。尽管已经积累了大量临床前证据,但仍需要更多研究来揭示可卡因调节成年海马神经发生(AHN)的机制,并确定这些成年新生神经元是否在与可卡因相关的行为中发挥作用,比如可卡因介导的认知症状。首先,本综述将总结可卡因诱导的多种神经生物学因素(神经递质、神经营养因子、糖皮质激素、炎症介质)的变化,这些因素可能在可卡因暴露后调节海马依赖性学习和成年海马神经发生。单独的一节将详细综述现有文献,这些文献对可卡因会减少成年海马神经发生这一普遍观点提出了挑战。事实上,可卡因具有短期抗增殖作用,但按照某些可卡因处理方案,成年新生的年轻神经元显然未受影响,甚至有所增加。因此,我们将尝试把这一证据与可卡因成瘾者中通常观察到的海马依赖性认知症状相协调,并提出未来研究的新方向以检验相关假设。基于此处给出的证据,成年海马神经发生的调节可能是可卡因塑造海马依赖性学习的众多机制之一。