Valenzuela C Fernando, Reid Natalie M, Blanco Benjamin B, Carlson Victoria L, Do Alynna B
Department of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Adv Exp Med Biol. 2025;1473:67-92. doi: 10.1007/978-3-031-81908-7_4.
This chapter comprehensively explores the impact of prenatal alcohol (ethanol) exposure (PAE) on the thalamus, integrating findings from animal models and human studies spanning various developmental stages. Animal model investigations, encompassing first and second trimester-equivalent exposures and the critical third trimester, where the brain growth spurt starts, reveal specific alterations in thalamic structures and circuits, emphasizing the specificity of damage to corticothalamic loops. The ventrobasal thalamic nucleus exhibits a unique response to PAE, involving intricate interactions with postnatal neurogenesis and neurotrophin responsiveness. Third trimester-equivalent exposure consistently induces apoptotic neurodegeneration in various thalamic nuclei, highlighting the heightened susceptibility of the visual thalamus, particularly the lateral geniculate nucleus, during critical developmental periods. The nucleus reuniens, vital for cognitive processes, was shown to be significantly affected by alcohol exposure during this period. Investigations into the trigeminal/somatosensory system activity revealed disruptions in glucose utilization and increased neuronal activity in the thalamus. Research on binge-like alcohol exposure during the brain growth spurt demonstrates lasting modifications in action-potential properties and synaptic currents in thalamic neurons projecting to the retrosplenial cortex. Human studies, employing advanced techniques like super-resolution fetal MRI and functional MRI, underscore the PAE-induced structural and functional consequences in the thalamus and its connections, spanning from fetal development to adulthood. The complex effects of PAE on thalamic structure and function vary across developmental stages, emphasizing the importance of considering factors such as age and concurrent exposures. The development of higher-resolution imaging tools is essential for assessing the impact of PAE on the structure and function of individual thalamic nuclei in humans.
本章全面探讨了产前酒精（乙醇）暴露（PAE）对丘脑的影响，整合了来自动物模型和涵盖不同发育阶段的人类研究结果。动物模型研究包括相当于孕早期和孕中期的暴露以及关键的孕晚期（大脑生长突增开始的时期），揭示了丘脑结构和回路的特定改变，强调了对皮质丘脑环路损伤的特异性。腹侧基底丘脑核表现出对PAE的独特反应，涉及与出生后神经发生和神经营养因子反应性的复杂相互作用。相当于孕晚期的暴露持续诱导各种丘脑核中的凋亡性神经变性，突出了在关键发育时期视觉丘脑，特别是外侧膝状体核的高度易感性。在此期间，对认知过程至关重要的 reunien 核被证明受到酒精暴露的显著影响。对三叉神经/体感系统活动的研究揭示了丘脑中葡萄糖利用的破坏和神经元活动的增加。对大脑生长突增期间暴饮样酒精暴露的研究表明，投射到压后皮质的丘脑神经元的动作电位特性和突触电流发生了持久改变。人类研究采用超分辨率胎儿MRI和功能MRI等先进技术，强调了PAE从胎儿发育到成年期在丘脑及其连接中诱导的结构和功能后果。PAE对丘脑结构和功能的复杂影响在不同发育阶段各不相同，强调了考虑年龄和同时暴露等因素的重要性。开发更高分辨率的成像工具对于评估PAE对人类个体丘脑核结构和功能的影响至关重要。
