Mira Rodrigo G, Lira Matias, Tapia-Rojas Cheril, Rebolledo Daniela L, Quintanilla Rodrigo A, Cerpa Waldo
Laboratorio de Función y Patología Neuronal, Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Laboratory of Neurobiology of Aging, Universidad San Sebastián, Santiago, Chile.
Front Behav Neurosci. 2020 Jan 24;13:288. doi: 10.3389/fnbeh.2019.00288. eCollection 2019.
Problematic alcohol drinking and alcohol dependence are an increasing health problem worldwide. Alcohol abuse is responsible for approximately 5% of the total deaths in the world, but addictive consumption of it has a substantial impact on neurological and memory disabilities throughout the population. One of the better-studied brain areas involved in cognitive functions is the hippocampus, which is also an essential brain region targeted by ethanol. Accumulated evidence in several rodent models has shown that ethanol treatment produces cognitive impairment in hippocampal-dependent tasks. These adverse effects may be related to the fact that ethanol impairs the cellular and synaptic plasticity mechanisms, including adverse changes in neuronal morphology, spine architecture, neuronal communication, and finally an increase in neuronal death. There is evidence that the damage that occurs in the different brain structures is varied according to the stage of development during which the subjects are exposed to ethanol, and even much earlier exposure to it would cause damage in the adult stage. Studies on the cellular and cognitive deficiencies produced by alcohol in the brain are needed in order to search for new strategies to reduce alcohol neuronal toxicity and to understand its consequences on memory and cognitive performance with emphasis on the crucial stages of development, including prenatal events to adulthood.
问题性饮酒和酒精依赖在全球范围内正成为日益严重的健康问题。酒精滥用约占全球总死亡人数的5%，但其成瘾性消费对整个人口的神经和记忆障碍有重大影响。海马体是参与认知功能且研究较多的脑区之一，也是乙醇作用的重要脑区。多个啮齿动物模型的累积证据表明，乙醇处理会导致海马体依赖性任务出现认知障碍。这些不良影响可能与乙醇损害细胞和突触可塑性机制有关，包括神经元形态、树突棘结构、神经元通讯的不良变化，最终导致神经元死亡增加。有证据表明，不同脑结构中发生的损伤会因受试者接触乙醇时的发育阶段而异，甚至更早接触乙醇也会在成年期造成损伤。为了寻找减少酒精神经元毒性的新策略，并了解其对记忆和认知表现的影响，尤其是在从产前到成年的关键发育阶段，需要对酒精在大脑中产生的细胞和认知缺陷进行研究。
